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1. A pan-respiratory antiviral chemotype targeting a transient host multi-protein complex.

Author: Michon, Maya, Müller-Schiffmann, Andreas, Lingappa, Anuradha, Yu, Shao, Du, Li, Deiter, Fred, Broce, Sean, Mallesh, Suguna, Crabtree, Jackelyn, Lingappa, Usha, Macieik, Amanda, Müller, Lisa, Ostermann, Philipp, Andrée, Marcel, Adams, Ortwin, Schaal, Heiner, Hogan, Robert, Tripp, Ralph, Appaiah, Umesh, Anand, Sanjeev, Campi, Thomas, Ford, Michael, Reed, Jonathan, Lin, Jim, Akintunde, Olayemi, Copeland, Kiel, Nichols, Christine, Petrouski, Emma, Moreira, Ana, Jiang, I-Ting, DeYarman, Nicholas, Brown, Ian, Lau, Sharon, Segal, Ilana, Goldsmith, Danielle, Hong, Shi, Asundi, Vinod, Briggs, Erica, Phyo, Ngwe, Froehlich, Markus, Onisko, Bruce, Matlack, Kent, Dey, Debendranath, Lingappa, Jaisri, Prasad, Dharma, Kitaygorodskyy, Anatoliy, Solas, Dennis, Boushey, Homer, Greenland, John, Pillai, Satish, Lo, Michael, Montgomery, Joel, Spiropoulou, Christina, Korth, Carsten, Selvarajah, Suganya, Paulvannan, Kumar, and Lingappa, Vishwanath
Subjects: allosteric modulator, drug discovery, host–viral interface, pan-respiratory antiviral therapeutics, phenotypic screen, viral capsid assembly, Antiviral Agents, Humans, Animals, 14-3-3 Proteins, Multiprotein Complexes, Host-Pathogen Interactions, Cell Line
Abstract: We present a novel small molecule antiviral chemotype that was identified by an unconventional cell-free protein synthesis and assembly-based phenotypic screen for modulation of viral capsid assembly. Activity of PAV-431, a representative compound from the series, has been validated against infectious viruses in multiple cell culture models for all six families of viruses causing most respiratory diseases in humans. In animals, this chemotype has been demonstrated efficacious for porcine epidemic diarrhoea virus (a coronavirus) and respiratory syncytial virus (a paramyxovirus). PAV-431 is shown to bind to the protein 14-3-3, a known allosteric modulator. However, it only appears to target the small subset of 14-3-3 which is present in a dynamic multi-protein complex whose components include proteins implicated in viral life cycles and in innate immunity. The composition of this target multi-protein complex appears to be modified upon viral infection and largely restored by PAV-431 treatment. An advanced analog, PAV-104, is shown to be selective for the virally modified target, thereby avoiding host toxicity. Our findings suggest a new paradigm for understanding, and drugging, the host-virus interface, which leads to a new clinical therapeutic strategy for treatment of respiratory viral disease.
Published: 2024

2. Systematic benchmarking of single-cell ATAC-sequencing protocols.

Author: De Rop, Florian, Hulselmans, Gert, Flerin, Chris, Soler-Vila, Paula, Rafels, Albert, Christiaens, Valerie, González-Blas, Carmen, Marchese, Domenica, Caratù, Ginevra, Poovathingal, Suresh, Rozenblatt-Rosen, Orit, Slyper, Michael, Luo, Wendy, Muus, Christoph, Duarte, Fabiana, Shrestha, Rojesh, Bagdatli, S, Corces, M, Mamanova, Lira, Knights, Andrew, Meyer, Kerstin, Mulqueen, Ryan, Taherinasab, Akram, Maschmeyer, Patrick, Pezoldt, Jörn, Lambert, Camille, Iglesias, Marta, Najle, Sebastián, Dossani, Zain, Martelotto, Luciano, Burkett, Zach, Lebofsky, Ronald, Martin-Subero, José, Pillai, Satish, Sebé-Pedrós, Arnau, Deplancke, Bart, Teichmann, Sarah, Ludwig, Leif, Braun, Theodore, Adey, Andrew, Greenleaf, William, Buenrostro, Jason, Regev, Aviv, Aerts, Stein, and Heyn, Holger
Subjects: Humans, Single-Cell Analysis, Benchmarking, Leukocytes, Mononuclear, Chromatin Immunoprecipitation Sequencing, Chromatin, Transposases, Sequence Analysis, DNA, High-Throughput Nucleotide Sequencing
Abstract: Single-cell assay for transposase-accessible chromatin by sequencing (scATAC-seq) has emerged as a powerful tool for dissecting regulatory landscapes and cellular heterogeneity. However, an exploration of systemic biases among scATAC-seq technologies has remained absent. In this study, we benchmark the performance of eight scATAC-seq methods across 47 experiments using human peripheral blood mononuclear cells (PBMCs) as a reference sample and develop PUMATAC, a universal preprocessing pipeline, to handle the various sequencing data formats. Our analyses reveal significant differences in sequencing library complexity and tagmentation specificity, which impact cell-type annotation, genotype demultiplexing, peak calling, differential region accessibility and transcription factor motif enrichment. Our findings underscore the importance of sample extraction, method selection, data processing and total cost of experiments, offering valuable guidance for future research. Finally, our data and analysis pipeline encompasses 169,000 PBMC scATAC-seq profiles and a best practices code repository for scATAC-seq data analysis, which are freely available to extend this benchmarking effort to future protocols.
Published: 2024

3. A viral assembly inhibitor blocks SARS-CoV-2 replication in airway epithelial cells.

Author: Du, Li, Deiter, Fred, Bouzidi, Mohamed, Billaud, Jean-Noël, Simmons, Graham, Dabral, Prerna, Selvarajah, Suganya, Lingappa, Anuradha, Michon, Maya, Yu, Shao, Paulvannan, Kumar, Manicassamy, Balaji, Lingappa, Vishwanath, Boushey, Homer, Greenland, John, and Pillai, Satish
Subjects: Humans, SARS-CoV-2, Virus Replication, Epithelial Cells, Antiviral Agents, Virus Assembly, COVID-19, COVID-19 Drug Treatment
Abstract: The ongoing evolution of SARS-CoV-2 to evade vaccines and therapeutics underlines the need for innovative therapies with high genetic barriers to resistance. Therefore, there is pronounced interest in identifying new pharmacological targets in the SARS-CoV-2 viral life cycle. The small molecule PAV-104, identified through a cell-free protein synthesis and assembly screen, was recently shown to target host protein assembly machinery in a manner specific to viral assembly. In this study, we investigate the capacity of PAV-104 to inhibit SARS-CoV-2 replication in human airway epithelial cells (AECs). We show that PAV-104 inhibits >99% of infection with diverse SARS-CoV-2 variants in immortalized AECs, and in primary human AECs cultured at the air-liquid interface (ALI) to represent the lung microenvironment in vivo. Our data demonstrate that PAV-104 inhibits SARS-CoV-2 production without affecting viral entry, mRNA transcription, or protein synthesis. PAV-104 interacts with SARS-CoV-2 nucleocapsid (N) and interferes with its oligomerization, blocking particle assembly. Transcriptomic analysis reveals that PAV-104 reverses SARS-CoV-2 induction of the type-I interferon response and the maturation of nucleoprotein signaling pathway known to support coronavirus replication. Our findings suggest that PAV-104 is a promising therapeutic candidate for COVID-19 with a mechanism of action that is distinct from existing clinical management approaches.
Published: 2024

4. The hypoxia-regulated ectonucleotidase CD73 is a host determinant of HIV latency

Author: Sperber, Hannah S, Raymond, Kyle A, Bouzidi, Mohamed S, Ma, Tongcui, Valdebenito, Silvana, Eugenin, Eliseo A, Roan, Nadia R, Deeks, Steven G, Winning, Sandra, Fandrey, Joachim, Schwarzer, Roland, and Pillai, Satish K
Subjects: Biological Sciences, Sexually Transmitted Infections, Infectious Diseases, HIV/AIDS, 2.1 Biological and endogenous factors, 2.2 Factors relating to the physical environment, Infection, Good Health and Well Being, Humans, Adenosine, CD4-Positive T-Lymphocytes, HIV Infections, HIV-1, Virus Activation, Virus Latency, Virus Replication, CD39, CD73, CP: Immunology, CP: Microbiology, HIV cure, IL-8, adenosine, eradication, hypoxia, lymphoid tissues, persistence, reservoir, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract: Deciphering the mechanisms underlying viral persistence is critical to achieving a cure for human immunodeficiency virus (HIV) infection. Here, we implement a systems approach to discover molecular signatures of HIV latently infected CD4+ T cells, identifying the immunosuppressive, adenosine-producing ectonucleotidase CD73 as a key surface marker of latent cells. Hypoxic conditioning, reflecting the lymphoid tissue microenvironment, increases the frequency of CD73+ CD4+ T cells and promotes HIV latency. Transcriptomic profiles of CD73+ CD4+ T cells favor viral quiescence, immune evasion, and cell survival. CD73+ CD4+ T cells are capable of harboring a functional HIV reservoir and reinitiating productive infection ex vivo. CD73 or adenosine receptor blockade facilitates latent HIV reactivation in vitro, mechanistically linking adenosine signaling to viral quiescence. Finally, tissue imaging of lymph nodes from HIV-infected individuals on antiretroviral therapy reveals spatial association between CD73 expression and HIV persistence in vivo. Our findings warrant development of HIV-cure strategies targeting the hypoxia-CD73-adenosine axis.
Published: 2023

5. Human galectin-9 potently enhances SARS-CoV-2 replication and inflammation in airway epithelial cells

Author: Du, Li, Bouzidi, Mohamed S, Gala, Akshay, Deiter, Fred, Billaud, Jean-Noël, Yeung, Stephen T, Dabral, Prerna, Jin, Jing, Simmons, Graham, Dossani, Zain Y, Niki, Toshiro, Ndhlovu, Lishomwa C, Greenland, John R, and Pillai, Satish K
Subjects: Biochemistry and Cell Biology, Biological Sciences, Coronaviruses, Lung, Emerging Infectious Diseases, Infectious Diseases, Clinical Research, Infection, Good Health and Well Being, Humans, Angiotensin-Converting Enzyme 2, COVID-19, Epithelial Cells, Galectins, Inflammation, SARS-CoV-2, Virus Replication, galectin-9, inflammation, airway epithelial cells, Biochemistry and cell biology, Immunology
Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has caused a global economic and health crisis. Recently, plasma levels of galectin-9 (Gal-9), a β-galactoside-binding lectin involved in immune regulation and viral immunopathogenesis, were reported to be elevated in the setting of severe COVID-19 disease. However, the impact of Gal-9 on SARS-CoV-2 infection and immunopathology remained to be elucidated. In this study, we demonstrate that Gal-9 treatment potently enhances SARS-CoV-2 replication in human airway epithelial cells (AECs), including immortalized AECs and primary AECs cultured at the air-liquid interface. Gal-9-glycan interactions promote SARS-CoV-2 attachment and entry into AECs in an angiotensin-converting enzyme 2 (ACE2)-dependent manner, enhancing the binding of the viral spike protein to ACE2. Transcriptomic analysis revealed that Gal-9 and SARS-CoV-2 infection synergistically induced the expression of key pro-inflammatory programs in AECs, including the IL-6, IL-8, IL-17, EIF2, and TNFα signaling pathways. Our findings suggest that manipulation of Gal-9 should be explored as a therapeutic strategy for SARS-CoV-2 infection.
Published: 2023

6. Host variation in type I interferon signaling genes (MX1), C-C chemokine receptor type 5 gene, and major histocompatibility complex class I alleles in treated HIV+ noncontrollers predict viral reservoir size.

Author: Siegel, David A, Thanh, Cassandra, Wan, Eunice, Hoh, Rebecca, Hobbs, Kristen, Pan, Tony, Gibson, Erica A, Kroetz, Deanna L, Martin, Jeffrey, Hecht, Frederick, Pilcher, Christopher, Martin, Maureen, Carrington, Mary, Pillai, Satish, Busch, Michael P, Stone, Mars, Levy, Claire N, Huang, Meei-Li, Roychoudhury, Pavitra, Hladik, Florian, Jerome, Keith R, Kiem, Hans-Peter, Henrich, Timothy J, Deeks, Steven G, and Lee, Sulggi A
Subjects: CD8-Positive T-Lymphocytes, Humans, HIV-1, HIV Infections, Interferon Type I, Histocompatibility Antigens Class I, HLA Antigens, Cross-Sectional Studies, Alleles, Myxovirus Resistance Proteins, Major Histocompatibility Complex, Receptors, Chemokine, RNA, Viral Load, Genetics, Infectious Diseases, Human Genome, HIV/AIDS, Aetiology, 2.1 Biological and endogenous factors, Infection, C-C chemokine receptor type 5 gene, HIV reservoir, host genetics, major histocompatibility complex class I, type I interferon, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology
Abstract: ObjectivePrior genomewide association studies have identified variation in major histocompatibility complex (MHC) class I alleles and C-C chemokine receptor type 5 gene (CCR5Δ32) as genetic predictors of viral control, especially in 'elite' controllers, individuals who remain virally suppressed in the absence of therapy.DesignCross-sectional genomewide association study.MethodsWe analyzed custom whole exome sequencing and direct human leukocyte antigen (HLA) typing from 202 antiretroviral therapy (ART)-suppressed HIV+ noncontrollers in relation to four measures of the peripheral CD4+ T-cell reservoir: HIV intact DNA, total (t)DNA, unspliced (us)RNA, and RNA/DNA. Linear mixed models were adjusted for potential covariates including age, sex, nadir CD4+ T-cell count, pre-ART HIV RNA, timing of ART initiation, and duration of ART suppression.ResultsPreviously reported 'protective' host genetic mutations related to viral setpoint (e.g. among elite controllers) were found to predict smaller HIV reservoir size. The HLA 'protective' B∗57:01 was associated with significantly lower HIV usRNA (q = 3.3 × 10-3), and among the largest subgroup, European ancestry individuals, the CCR5Δ32 deletion was associated with smaller HIV tDNA (P = 4.3 × 10-3) and usRNA (P = 8.7 × 10-3). In addition, genomewide analysis identified several single nucleotide polymorphisms in MX1 (an interferon stimulated gene) that were significantly associated with HIV tDNA (q = 0.02), and the direction of these associations paralleled MX1 gene eQTL expression.ConclusionsWe observed a significant association between previously reported 'protective' MHC class I alleles and CCR5Δ32 with the HIV reservoir size in noncontrollers. We also found a novel association between MX1 and HIV total DNA (in addition to other interferon signaling relevant genes, PPP1CB, DDX3X). These findings warrant further investigation in future validation studies.
Published: 2023

7. Galectin-9 protects humanized-ACE2 immunocompetent mice from SARS-CoV-2 infection.

Author: Yeung, Stephen, Premeaux, Thomas, Du, Li, Niki, Toshiro, Pillai, Satish, Khanna, Kamal, and Ndhlovu, Lishomwa
Subjects: COVID-19, SARS-CoV-2, galectin-9, inflammation, lectins, Mice, Humans, Animals, COVID-19, Angiotensin-Converting Enzyme 2, SARS-CoV-2, Mice, Transgenic, Galectins
Abstract: SARS-CoV-2 remains a global health crisis even with effective vaccines and the availability of FDA approved therapies. Efforts to understand the complex disease pathology and develop effective strategies to limit mortality and morbidity are needed. Recent studies reveal circulating Galectin-9 (gal-9), a soluble beta-galactoside binding lectin with immunoregulatory properties, are elevated in SARS-CoV-2 infected individuals with moderate to severe disease. Moreover, in silico studies demonstrate gal-9 can potentially competitively bind the ACE2 receptor on susceptible host cells. Here, we determined whether early introduction of exogenous gal-9 following SARS-CoV-2 infection in humanized ACE2 transgenic mice (K18-hACE2) may reduce disease severity. Mice were infected and treated with a single dose of a human recombinant form of gal-9 (rh-gal-9) and monitored for morbidity. Subgroups of mice were humanely euthanized at 2- and 5- days post infection (dpi) for viral levels by plaque assay, immune changes measures by flow cytometry, and soluble mediators by protein analysis from lung tissue and bronchoalveolar Lavage fluid (BALF). Mice treated with rh-gal-9 during acute infection had improved survival compared to PBS treated controls. At 5 dpi, rh-gal-9 treated mice had enhanced viral clearance in the BALF, but not in the lung parenchyma. Increased T and dendritic cells and decreased neutrophil frequencies in the lung at 5 dpi were observed, whereas BALF had elevated levels of type-I interferons and proinflammatory cytokines. These results suggest a role for rh-gal-9 in limiting acute COVID-19. Further studies are required to determine the optimal design of gal-9 treatment to effectively ameliorate COVID-19 disease.
Published: 2022

8. Elevated Galectin-9 across the human brain correlates with HIV neuropathology and detrimental cognitive states

Author: Premeaux, Thomas A., Yeung, Stephen T., Pillai, Satish K., and Ndhlovu, Lishomwa C.
Published: 2023
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9. Hyaluronic acid is a negative regulator of mucosal fibroblast-mediated enhancement of HIV infection

Author: Egedal, Johanne H, Xie, Guorui, Packard, Thomas A, Laustsen, Anders, Neidleman, Jason, Georgiou, Konstantinos, Pillai, Satish K, Greene, Warner C, Jakobsen, Martin R, and Roan, Nadia R
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Infectious Diseases, HIV/AIDS, 2.1 Biological and endogenous factors, Inflammatory and immune system, Infection, Biomarkers, CD4-Positive T-Lymphocytes, Disease Susceptibility, Extracellular Matrix, Fibroblasts, Gene Expression Regulation, Gene Knockdown Techniques, HIV Infections, HIV-1, Host-Pathogen Interactions, Humans, Hyaluronan Synthases, Hyaluronic Acid, Mucous Membrane, Biological Sciences, Medical and Health Sciences
Abstract: The majority of HIV infections are established through the genital or rectal mucosa. Fibroblasts are abundant in these tissues, and although not susceptible to infection, can potently enhance HIV infection of CD4+ T cells. Hyaluronic acid (HA) is a major component of the extracellular matrix of fibroblasts, and its levels are influenced by the inflammatory state of the tissue. Since inflammation is known to facilitate HIV sexual transmission, we investigated the role of HA in genital mucosal fibroblast-mediated enhancement of HIV infection. Depletion of HA by CRISPR-Cas9 in primary foreskin fibroblasts augmented the ability of the fibroblasts to increase HIV infection of CD4+ T cells. This amplified enhancement required direct contact between the fibroblasts and CD4+ T cells, and could be attributed to both increased rates of trans-infection and the increased ability of HA-deficient fibroblasts to push CD4+ T cells into a state of higher permissivity to infection. This HIV-permissive state was characterized by differential expression of genes associated with regulation of cell metabolism and death. Our results suggest that conditions resulting in diminished cell-surface HA on fibroblasts, such as genital inflammation, can promote HIV transmission by conditioning CD4+ T cells toward a state more vulnerable to infection by HIV.
Published: 2021

10. Efficient generation of isogenic primary human myeloid cells using CRISPR-Cas9 ribonucleoproteins

Author: Hiatt, Joseph, Cavero, Devin A, McGregor, Michael J, Zheng, Weihao, Budzik, Jonathan M, Roth, Theodore L, Haas, Kelsey M, Wu, David, Rathore, Ujjwal, Meyer-Franke, Anke, Bouzidi, Mohamed S, Shifrut, Eric, Lee, Youjin, Kumar, Vigneshwari Easwar, Dang, Eric V, Gordon, David E, Wojcechowskyj, Jason A, Hultquist, Judd F, Fontaine, Krystal A, Pillai, Satish K, Cox, Jeffery S, Ernst, Joel D, Krogan, Nevan J, and Marson, Alexander
Subjects: Biological Sciences, Genetics, Infectious Diseases, Biotechnology, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, 4.1 Discovery and preclinical testing of markers and technologies, Animals, CRISPR-Cas Systems, Genome, Humans, Mice, Myeloid Cells, Ribonucleoproteins, CRISPR, Cas9, dendritic cells, electroporation, host-pathogen interactions, knockout, macrophages, monocytes, myeloid cells, ribonculeoproteins, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract: Genome engineering of primary human cells with CRISPR-Cas9 has revolutionized experimental and therapeutic approaches to cell biology, but human myeloid-lineage cells have remained largely genetically intractable. We present a method for the delivery of CRISPR-Cas9 ribonucleoprotein (RNP) complexes by nucleofection directly into CD14+ human monocytes purified from peripheral blood, leading to high rates of precise gene knockout. These cells can be efficiently differentiated into monocyte-derived macrophages or dendritic cells. This process yields genetically edited cells that retain transcript and protein markers of myeloid differentiation and phagocytic function. Genetic ablation of the restriction factor SAMHD1 increased HIV-1 infection >50-fold, demonstrating the power of this system for genotype-phenotype interrogation. This fast, flexible, and scalable platform can be used for genetic studies of human myeloid cells in immune signaling, inflammation, cancer immunology, host-pathogen interactions, and beyond, and could facilitate the development of myeloid cellular therapies.
Published: 2021

11. Evaluating a New Class of AKT/mTOR Activators for HIV Latency-Reversing Activity Ex Vivo and In Vivo

Author: Gramatica, Andrea, Schwarzer, Roland, Brantley, William, Varco-Merth, Benjamin, Sperber, Hannah S, Hull, Philip A, Montano, Mauricio, Migueles, Stephen A, Rosenthal, Danielle, Hogan, Louise E, Johnson, Jeffrey R, Packard, Thomas A, Grimmett, Zachary W, Herzig, Eytan, Besnard, Emilie, Nekorchuk, Michael, Hsiao, Feng, Deeks, Steven G, Snape, Michael, Kiernan, Bernard, Roan, Nadia R, Lifson, Jeffrey D, Estes, Jacob D, Picker, Louis J, Verdin, Eric, Krogan, Nevan J, Henrich, Timothy J, Connors, Mark, Ott, Melanie, Pillai, Satish K, Okoye, Afam A, and Greene, Warner C
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Immunotherapy, HIV/AIDS, Infectious Diseases, 5.1 Pharmaceuticals, Good Health and Well Being, HIV cure, HIV-1, HIV latency reversion, SIV, in vivo study, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract: An ability to activate latent HIV-1 expression could benefit many HIV cure strategies, but the first generation of latency reversing agents (LRAs) has proven disappointing. We evaluated AKT/mTOR activators as a potential new class of LRAs. Two glycogen synthase kinase-3 inhibitors (GSK-3i's), SB-216763 and tideglusib (the latter already in phase II clinical trials) that activate AKT/mTOR signaling were tested. These GSK-3i's reactivated latent HIV-1 present in blood samples from aviremic individuals on antiretroviral therapy (ART) in the absence of T cell activation, release of inflammatory cytokines, cell toxicity, or impaired effector function of cytotoxic T lymphocytes or NK cells. However, when administered in vivo to SIV-infected rhesus macaques on suppressive ART, tideglusib exhibited poor pharmacodynamic properties and resulted in no clear evidence of significant SIV latency reversal. Whether alternative pharmacological formulations or combinations of this drug with other classes of LRAs will lead to an effective in vivo latency-reversing strategy remains to be determined.IMPORTANCE If combined with immune therapeutics, latency reversing agents (LRAs) have the potential to reduce the size of the reservoir sufficiently that an engineered immune response can control the virus in the absence of antiretroviral therapy. We have identified a new class of LRAs that do not induce T-cell activation and that are able to potentiate, rather than inhibit, CD8+ T and NK cell cytotoxic effector functions. This new class of LRAs corresponds to inhibitors of glycogen synthase kinase-3. In this work, we have also studied the effects of one member of this drug class, tideglusib, in SIV-infected rhesus monkeys. When tested in vivo, however, tideglusib showed unfavorable pharmacokinetic properties, which resulted in lack of SIV latency reversal. The disconnect between our ex vivo and in vivo results highlights the importance of developing next generation LRAs with pharmacological properties that allow systemic drug delivery in relevant anatomical compartments harboring latent reservoirs.
Published: 2021

12. TCF-1 regulates HIV-specific CD8+ T cell expansion capacity

Author: Rutishauser, Rachel L, Deguit, Christian Deo T, Hiatt, Joseph, Blaeschke, Franziska, Roth, Theodore L, Wang, Lynn, Raymond, Kyle A, Starke, Carly E, Mudd, Joseph C, Chen, Wenxuan, Smullin, Carolyn P, Matus-Nicodemos, Rodrigo, Hoh, Rebecca, Krone, Melissa R, Hecht, Frederick M, Pilcher, Christopher D, Martin, Jeffrey N, Koup, Richard A, Douek, Daniel C, Brenchley, Jason M, Sékaly, Rafick-Pierre, Pillai, Satish K, Marson, Alexander, Deeks, Steven G, McCune, Joseph M, and Hunt, Peter W
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, HIV/AIDS, Infectious Diseases, Sexually Transmitted Infections, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Infection, Good Health and Well Being, Adult, Aged, Animals, CD8-Positive T-Lymphocytes, Female, Gene Knockout Techniques, HIV Antigens, HIV Infections, HIV-1, Humans, Immunologic Memory, Macaca mulatta, Male, Middle Aged, Simian Acquired Immunodeficiency Syndrome, Simian Immunodeficiency Virus, T Cell Transcription Factor 1, Viral Load, Simian immunodeficiency virus, AIDS/HIV, Adaptive immunity, T cells, Biomedical and clinical sciences, Health sciences
Abstract: Although many HIV cure strategies seek to expand HIV-specific CD8+ T cells to control the virus, all are likely to fail if cellular exhaustion is not prevented. A loss in stem-like memory properties (i.e., the ability to proliferate and generate secondary effector cells) is a key feature of exhaustion; little is known, however, about how these properties are regulated in human virus-specific CD8+ T cells. We found that virus-specific CD8+ T cells from humans and nonhuman primates naturally controlling HIV/SIV infection express more of the transcription factor TCF-1 than noncontrollers. HIV-specific CD8+ T cell TCF-1 expression correlated with memory marker expression and expansion capacity and declined with antigenic stimulation. CRISPR-Cas9 editing of TCF-1 in human primary T cells demonstrated a direct role in regulating expansion capacity. Collectively, these data suggest that TCF-1 contributes to the regulation of the stem-like memory property of secondary expansion capacity of HIV-specific CD8+ T cells, and they provide a rationale for exploring the enhancement of this pathway in T cell-based therapeutic strategies for HIV.
Published: 2021

13. μ‐Lat: A mouse model to evaluate human immunodeficiency virus eradication strategies

Author: Sperber, Hannah S, Togarrati, Padma Priya, Raymond, Kyle A, Bouzidi, Mohamed S, Gilfanova, Renata, Gutierrez, Alan G, Muench, Marcus O, and Pillai, Satish K
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, HIV/AIDS, Infectious Diseases, Infection, Animals, Bone Marrow, Cell Transplantation, Disease Models, Animal, Female, Green Fluorescent Proteins, HIV, HIV Infections, Humans, Jurkat Cells, Lung, Male, Mice, Mice, Inbred NOD, Proviruses, Spleen, Transfection, Virus Latency, antiviral gene therapy, humanized mouse, HIV latency, latency reversal, shock and kill, Biochemistry and Cell Biology, Physiology, Medical Physiology, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical physiology
Abstract: A critical barrier to the development of a human immunodeficiency virus (HIV) cure is the lack of a scalable animal model that enables robust evaluation of eradication approaches prior to testing in humans. We established a humanized mouse model of latent HIV infection by transplanting "J-Lat" cells, Jurkat cells harboring a latent HIV provirus encoding an enhanced green fluorescent protein (GFP) reporter, into irradiated adult NOD.Cg-Prkdcscid Il2rgtm1Wjl /SzJ (NSG) mice. J-Lat cells exhibited successful engraftment in several tissues including spleen, bone barrow, peripheral blood, and lung, in line with the diverse natural tissue tropism of HIV. Administration of tumor necrosis factor (TNF)-α, an established HIV latency reversal agent, significantly induced GFP expression in engrafted cells across tissues, reflecting viral reactivation. These data suggest that our murine latency ("μ-Lat") model enables efficient determination of how effectively viral eradication agents, including latency reversal agents, penetrate, and function in diverse anatomical sites harboring HIV in vivo.
Published: 2020

14. SARS-CoV-2 seroprevalence and neutralizing activity in donor and patient blood.

Author: Ng, Dianna L, Goldgof, Gregory M, Shy, Brian R, Levine, Andrew G, Balcerek, Joanna, Bapat, Sagar P, Prostko, John, Rodgers, Mary, Coller, Kelly, Pearce, Sandra, Franz, Sergej, Du, Li, Stone, Mars, Pillai, Satish K, Sotomayor-Gonzalez, Alicia, Servellita, Venice, Martin, Claudia Sanchez San, Granados, Andrea, Glasner, Dustin R, Han, Lucy M, Truong, Kent, Akagi, Naomi, Nguyen, David N, Neumann, Neil M, Qazi, Daniel, Hsu, Elaine, Gu, Wei, Santos, Yale A, Custer, Brian, Green, Valerie, Williamson, Phillip, Hills, Nancy K, Lu, Chuanyi M, Whitman, Jeffrey D, Stramer, Susan L, Wang, Candace, Reyes, Kevin, Hakim, Jill MC, Sujishi, Kirk, Alazzeh, Fariba, Pham, Lori, Thornborrow, Edward, Oon, Ching-Ying, Miller, Steve, Kurtz, Theodore, Simmons, Graham, Hackett, John, Busch, Michael P, and Chiu, Charles Y
Subjects: Humans, Pneumonia, Viral, Coronavirus Infections, Immunoglobulin G, Immunoglobulin M, Antibodies, Viral, Serologic Tests, Clinical Laboratory Techniques, Sensitivity and Specificity, Seroepidemiologic Studies, San Francisco, Antibodies, Neutralizing, Pandemics, Betacoronavirus, COVID-19, SARS-CoV-2, COVID-19 Testing, Pneumonia, Viral, Antibodies, Neutralizing
Abstract: Given the limited availability of serological testing to date, the seroprevalence of SARS-CoV-2-specific antibodies in different populations has remained unclear. Here, we report very low SARS-CoV-2 seroprevalence in two San Francisco Bay Area populations. Seroreactivity was 0.26% in 387 hospitalized patients admitted for non-respiratory indications and 0.1% in 1,000 blood donors in early April 2020. We additionally describe the longitudinal dynamics of immunoglobulin-G (IgG), immunoglobulin-M (IgM), and in vitro neutralizing antibody titers in COVID-19 patients. The median time to seroconversion ranged from 10.3-11.0 days for these 3 assays. Neutralizing antibodies rose in tandem with immunoglobulin titers following symptom onset, and positive percent agreement between detection of IgG and neutralizing titers was >93%. These findings emphasize the importance of using highly accurate tests for surveillance studies in low-prevalence populations, and provide evidence that seroreactivity using SARS-CoV-2 anti-nucleocapsid protein IgG and anti-spike IgM assays are generally predictive of in vitro neutralizing capacity.
Published: 2020

15. FOXO1 promotes HIV latency by suppressing ER stress in T cells

Author: Vallejo-Gracia, Albert, Chen, Irene P, Perrone, Rosalba, Besnard, Emilie, Boehm, Daniela, Battivelli, Emilie, Tezil, Tugsan, Krey, Karsten, Raymond, Kyle A, Hull, Philip A, Walter, Marius, Habrylo, Ireneusz, Cruz, Andrew, Deeks, Steven, Pillai, Satish, Verdin, Eric, and Ott, Melanie
Subjects: Microbiology, Biological Sciences, Infectious Diseases, HIV/AIDS, Sexually Transmitted Infections, 2.1 Biological and endogenous factors, Infection, Activating Transcription Factor 4, CD4-Positive T-Lymphocytes, Endoplasmic Reticulum Stress, Forkhead Box Protein O1, Gene Knockdown Techniques, HIV Infections, HIV-1, Humans, K562 Cells, Virus Activation, Virus Latency, Medical Microbiology
Abstract: Quiescence is a hallmark of CD4+ T cells latently infected with human immunodeficiency virus 1 (HIV-1). While reversing this quiescence is an effective approach to reactivate latent HIV from T cells in culture, it can cause deleterious cytokine dysregulation in patients. As a key regulator of T-cell quiescence, FOXO1 promotes latency and suppresses productive HIV infection. We report that, in resting T cells, FOXO1 inhibition impaired autophagy and induced endoplasmic reticulum (ER) stress, thereby activating two associated transcription factors: activating transcription factor 4 (ATF4) and nuclear factor of activated T cells (NFAT). Both factors associate with HIV chromatin and are necessary for HIV reactivation. Indeed, inhibition of protein kinase R-like ER kinase, an ER stress sensor that can mediate the induction of ATF4, and calcineurin, a calcium-dependent regulator of NFAT, synergistically suppressed HIV reactivation induced by FOXO1 inhibition. Thus, our studies uncover a link of FOXO1, ER stress and HIV infection that could be therapeutically exploited to selectively reverse T-cell quiescence and reduce the size of the latent viral reservoir.
Published: 2020

16. Seminal Plasma-Derived Extracellular-Vesicle Fractions from HIV-Infected Men Exhibit Unique MicroRNA Signatures and Induce a Proinflammatory Response in Cells Isolated from the Female Reproductive Tract

Author: de Menezes, Erika G Marques, Jang, Karen, George, Ashley F, Nyegaard, Mette, Neidleman, Jason, Inglis, Heather C, Danesh, Ali, Deng, Xutao, Afshari, Amirali, Kim, Young H, Billaud, Jean-Noël, Marson, Kara, Pilcher, Christopher D, Pillai, Satish K, Norris, Philip J, and Roan, Nadia R
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Clinical Research, Infectious Diseases, Prevention, Sexually Transmitted Infections, HIV/AIDS, Biotechnology, Genetics, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Adult, Cohort Studies, Cytokines, Extracellular Vesicles, Female, Genitalia, Female, HIV Infections, HIV-1, Humans, Male, MicroRNAs, Semen, Sexual Behavior, Transcriptome, extracellular vesicles, epithelial cells, female reproductive tract, human immunodeficiency virus, miRNAs, seminal plasma, stromal fibroblasts, transcription, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract: The continuing spread of HIV/AIDS is predominantly fueled by sexual exposure to HIV-contaminated semen. Seminal plasma (SP), the liquid portion of semen, harbors a variety of factors that may favor HIV transmission by facilitating viral entry into host cells, eliciting the production of proinflammatory cytokines, and enhancing the translocation of HIV across the genital epithelium. One important and abundant class of factors in SP is extracellular vesicles (EVs), which, in general, are important intercellular signal transducers. Although numerous studies have characterized blood plasma-derived EVs from both uninfected and HIV-infected individuals, little is known about the properties of EVs from the semen of HIV-infected individuals. We report here that fractionated SP enriched for EVs from HIV-infected men induces potent transcriptional responses in epithelial and stromal cells that interface with the luminal contents of the female reproductive tract. Semen EV fractions from acutely infected individuals induced a more proinflammatory signature than those from uninfected individuals. This was not associated with any observable differences in the surface phenotypes of the vesicles. However, microRNA (miRNA) expression profiling analysis revealed that EV fractions from infected individuals exhibit a broader and more diverse profile than those from uninfected individuals. Taken together, our data suggest that SP EVs from HIV-infected individuals exhibit unique miRNA signatures and exert potent proinflammatory transcriptional changes in cells of the female reproductive tract, which may facilitate HIV transmission.IMPORTANCE Seminal plasma (SP), the major vehicle for HIV, can modulate HIV transmission risk through a variety of mechanisms. Extracellular vesicles (EVs) are extremely abundant in semen, and because they play a key role in intercellular communication pathways and immune regulation, they may impact the likelihood of HIV transmission. However, little is known about the properties and signaling effects of SP-derived EVs in the context of HIV transmission. Here, we conduct a phenotypic, transcriptomic, and functional characterization of SP and SP-derived EVs from uninfected and HIV-infected men. We find that both SP and its associated EVs elicit potent proinflammatory transcriptional responses in cells that line the genital tract. EVs from HIV-infected men exhibit a more diverse repertoire of miRNAs than EVs from uninfected men. Our findings suggest that EVs from the semen of HIV-infected men may significantly impact the likelihood of HIV transmission through multiple mechanisms.
Published: 2020

17. SARS-CoV-2 seroprevalence and neutralizing activity in donor and patient blood from the San Francisco Bay Area.

Author: Ng, Dianna, Goldgof, Gregory, Shy, Brian, Levine, Andrew, Balcerek, Joanna, Bapat, Sagar, Prostko, John, Rodgers, Mary, Coller, Kelly, Pearce, Sandra, Franz, Sergej, Du, Li, Stone, Mars, Pillai, Satish, Sotomayor-Gonzalez, Alicia, Servellita, Venice, Sanchez-San Martin, Claudia, Granados, Andrea, Glasner, Dustin, Han, Lucy, Truong, Kent, Akagi, Naomi, Nguyen, David, Neumann, Neil, Qazi, Daniel, Hsu, Elaine, Gu, Wei, Santos, Yale, Custer, Brian, Green, Valerie, Williamson, Phillip, Hills, Nancy, Lu, Chuanyi, Whitman, Jeffrey, Stramer, Susan, Wang, Candace, Reyes, Kevin, Hakim, Jill, Sujishi, Kirk, Alazzeh, Fariba, Pharm, Lori, Oon, Ching-Ying, Miller, Steve, Kurtz, Theodore, Hackett, John, Simmons, Graham, Busch, Michael, and Chiu, Charles
Abstract: We report very low SARS-CoV-2 seroprevalence in two San Francisco Bay Area populations. Seropositivity was 0.26% in 387 hospitalized patients admitted for non-respiratory indications and 0.1% in 1,000 blood donors. We additionally describe the longitudinal dynamics of immunoglobulin-G, immunoglobulin-M, and in vitro neutralizing antibody titers in COVID-19 patients. Neutralizing antibodies rise in tandem with immunoglobulin levels following symptom onset, exhibiting median time to seroconversion within one day of each other, and there is >93% positive percent agreement between detection of immunoglobulin-G and neutralizing titers.
Published: 2020

18. Enhanced Adenovirus Vaccine Safety Surveillance in Military Setting, United States

Author: Iskander, John, Blanchet, Scott, Springer, Caitlin, Rockwell, Patrick, Thomas, Dana, and Pillai, Satish
Subjects: United States. Coast Guard Academy -- Health aspects, Military personnel -- Health aspects, Adenovirus diseases -- Prevention -- Risk factors, Viral vaccines -- Patient outcomes, Health
Abstract: Adenovirus infection results in considerable illness among congregate military populations (1). US Food and Drug Administration-approved use of a live, oral, bivalent adenovirus vaccine for military populations began in 2011 [...]
Published: 2023

19. Elevated cerebrospinal fluid Galectin-9 is associated with central nervous system immune activation and poor cognitive performance in older HIV-infected individuals

Author: Premeaux, Thomas A, D’Antoni, Michelle L, Abdel-Mohsen, Mohamed, Pillai, Satish K, Kallianpur, Kalpana J, Nakamoto, Beau K, Agsalda-Garcia, Melissa, Shiramizu, Bruce, Shikuma, Cecilia M, Gisslén, Magnus, Price, Richard W, Valcour, Victor, and Ndhlovu, Lishomwa C
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Clinical Research, Mental Health, Neurodegenerative, Neurosciences, Brain Disorders, HIV/AIDS, Acquired Cognitive Impairment, Behavioral and Social Science, Sexually Transmitted Infections, Aging, 2.1 Biological and endogenous factors, Infection, Neurological, Adult, Age Factors, Anti-HIV Agents, Antigens, CD, Antigens, Differentiation, Myelomonocytic, Antiretroviral Therapy, Highly Active, Biomarkers, Case-Control Studies, Central Nervous System, Cognition, Female, Galectins, HIV Infections, HIV-1, Humans, Male, Middle Aged, Neopterin, Neuropsychological Tests, RNA, Viral, Receptors, Cell Surface, Viremia, Galectin-9, HIV, Neuroinflammation, Cognitive disorders, Clinical Sciences, Virology, Clinical sciences, Medical microbiology
Abstract: We previously reported that galectin-9 (Gal-9), a soluble lectin with immunomodulatory properties, is elevated in plasma during HIV infection and induces HIV transcription. The link between Gal-9 and compromised neuronal function is becoming increasingly evident; however, the association with neuroHIV remains unknown. We measured Gal-9 levels by ELISA in cerebrospinal fluid (CSF) and plasma of 70 HIV-infected (HIV+) adults stratified by age (older > 40 years and younger
Published: 2019

20. Alternative Methods for Grouping Race and Ethnicity to Monitor COVID-19 Outcomes and Vaccination Coverage

Author: Yoon, Paula, Hall, Jeffrey, Fuld, Jennifer, Mattocks, S. Linda, Lyons, B. Casey, Bhatkoti, Roma, Henley, Jane, McNaghten, A.D., Daskalakis, Demetre, and Pillai, Satish K.
Published: 2021

21. Reiterative Enrichment and Authentication of CRISPRi Targets (REACT) identifies the proteasome as a key contributor to HIV-1 latency.

Author: Li, Zichong, Wu, Jun, Chavez, Leonard, Hoh, Rebecca, Deeks, Steven G, Pillai, Satish K, and Zhou, Qiang
Subjects: CD4-Positive T-Lymphocytes, Cell Line, Jurkat Cells, Humans, HIV-1, HIV Infections, HIV Seropositivity, Proteasome Endopeptidase Complex, Transcriptional Elongation Factors, Anti-HIV Agents, Virus Latency, Virus Activation, Proteasome Inhibitors, CRISPR-Cas Systems, Clustered Regularly Interspaced Short Palindromic Repeats, Gene Editing, Virology, Microbiology, Immunology, Medical Microbiology
Abstract: The establishment of HIV-1 latency gives rise to persistent chronic infection that requires life-long treatment. To reverse latency for viral eradiation, the HIV-1 Tat protein and its associated ELL2-containing Super Elongation Complexes (ELL2-SECs) are essential to activate HIV-1 transcription. Despite efforts to identify effective latency-reversing agents (LRA), avenues for exposing latent HIV-1 remain inadequate, prompting the need to identify novel LRA targets. Here, by conducting a CRISPR interference-based screen to reiteratively enrich loss-of-function genotypes that increase HIV-1 transcription in latently infected CD4+ T cells, we have discovered a key role of the proteasome in maintaining viral latency. Downregulating or inhibiting the proteasome promotes Tat-transactivation in cell line models. Furthermore, the FDA-approved proteasome inhibitors bortezomib and carfilzomib strongly synergize with existing LRAs to reactivate HIV-1 in CD4+ T cells from antiretroviral therapy-suppressed individuals without inducing cell activation or proliferation. Mechanistically, downregulating/inhibiting the proteasome elevates the levels of ELL2 and ELL2-SECs to enable Tat-transactivation, indicating the proteasome-ELL2 axis as a key regulator of HIV-1 latency and promising target for therapeutic intervention.
Published: 2019

22. Distinct chromatin functional states correlate with HIV latency reactivation in infected primary CD4+ T cells.

Author: Battivelli, Emilie, Dahabieh, Matthew S, Abdel-Mohsen, Mohamed, Svensson, J Peter, Tojal Da Silva, Israel, Cohn, Lillian B, Gramatica, Andrea, Deeks, Steven, Greene, Warner C, Pillai, Satish K, and Verdin, Eric
Subjects: CD4-Positive T-Lymphocytes, Cells, Cultured, Chromatin, Humans, HIV-1, Virion, HIV Infections, Virus Integration, Virus Latency, Virus Activation, HIV-1 latency, human, infectious disease, integration sites, latency reversal, latency reversing agents, microbiology, reservoirs, Cells, Cultured, Biochemistry and Cell Biology
Abstract: Human immunodeficiency virus (HIV) infection is currently incurable, due to the persistence of latently infected cells. The 'shock and kill' approach to a cure proposes to eliminate this reservoir via transcriptional activation of latent proviruses, enabling direct or indirect killing of infected cells. Currently available latency-reversing agents (LRAs) have however proven ineffective. To understand why, we used a novel HIV reporter strain in primary CD4+ T cells and determined which latently infected cells are reactivatable by current candidate LRAs. Remarkably, none of these agents reactivated more than 5% of cells carrying a latent provirus. Sequencing analysis of reactivatable vs. non-reactivatable populations revealed that the integration sites were distinguishable in terms of chromatin functional states. Our findings challenge the feasibility of 'shock and kill', and suggest the need to explore other strategies to control the latent HIV reservoir.
Published: 2018

23. Granulocyte-Derived Extracellular Vesicles Activate Monocytes and Are Associated With Mortality in Intensive Care Unit Patients

Author: Danesh, Ali, Inglis, Heather C, Abdel-Mohsen, Mohamed, Deng, Xutao, Adelman, Avril, Schechtman, Kenneth B, Heitman, John W, Vilardi, Ryan, Shah, Avani, Keating, Sheila M, Cohen, Mitchell J, Jacobs, Evan S, Pillai, Satish K, Lacroix, Jacques, Spinella, Philip C, and Norris, Philip J
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Good Health and Well Being, Biomarkers, Critical Illness, Cytokines, Extracellular Vesicles, Gene Expression Profiling, Granulocyte-Macrophage Colony-Stimulating Factor, Granulocytes, High-Throughput Nucleotide Sequencing, Hospital Mortality, Humans, Intensive Care Units, Macrophages, Monocytes, Risk Factors, Transforming Growth Factor beta, extracellular vesicles, monocytes, granulocytes, exosomes, microvesicles, mortality, intensive care unit, receptor, Immunology, Medical Microbiology, Biochemistry and cell biology, Genetics
Abstract: To understand how extracellular vesicle (EV) subtypes differentially activate monocytes, a series of in vitro studies were performed. We found that plasma-EVs biased monocytes toward an M1 profile. Culturing monocytes with granulocyte-, monocyte-, and endothelial-EVs induced several pro-inflammatory cytokines. By contrast, platelet-EVs induced TGF-β and GM-CSF, and red blood cell (RBC)-EVs did not activate monocytes in vitro. The scavenger receptor CD36 was important for binding of RBC-EVs to monocytes, while blockade of CD36, CD163, CD206, TLR1, TLR2, and TLR4 did not affect binding of plasma-EVs to monocytes in vitro. To identify mortality risk factors, multiple soluble factors and EV subtypes were measured in patients' plasma at intensive care unit admission. Of 43 coagulation factors and cytokines measured, two were significantly associated with mortality, tissue plasminogen activator and cystatin C. Of 14 cellular markers quantified on EVs, 4 were early predictors of mortality, including the granulocyte marker CD66b. In conclusion, granulocyte-EVs have potent pro-inflammatory effects on monocytes in vitro. Furthermore, correlation of early granulocyte-EV levels with mortality in critically ill patients provides a potential target for intervention in management of the pro-inflammatory cascade associated with critical illness.
Published: 2018

24. Absence of neurocognitive disadvantage associated with paediatric HIV subtype A infection in children on antiretroviral therapy.

Author: Bangirana, Paul, Ruel, Theodore D, Boivin, Michael J, Pillai, Satish K, Giron, Leila B, Sikorskii, Alla, Banik, Asish, and Achan, Jane
Subjects: Leukocytes, Mononuclear, Humans, HIV, HIV Infections, Reverse Transcriptase Inhibitors, Anti-HIV Agents, CD4 Lymphocyte Count, Child, Child, Preschool, Uganda, Female, Male, Lopinavir, Neurocognitive Disorders, HIV subtype, antiretroviral therapy, children, neurocognition, Leukocytes, Mononuclear, Preschool, Clinical Sciences, Public Health and Health Services, Other Medical and Health Sciences
Abstract: IntroductionInfection with HIV subtype A has been associated with poorer neurocognitive outcomes compared to HIV subtype D in Ugandan children not eligible for antiretroviral therapy (ART). In this study, we sought to determine whether subtype-specific differences are also observed among children receiving ART.Materials and methodsChildren were recruited from a clinical trial in which they were randomized to receive either lopinavir (LPV)- or non-nucleoside reverse transcriptase inhibitor (NNRTI)- based ART (NCT00978068). Age at initiation of ART ranged from six months to six years. HIV subtype was determined by PCR amplification and population sequencing of the pol region derived from peripheral blood mononuclear cell DNA, followed by application of the REGA and Recombinant Identification Programme algorithms. General cognition was assessed using the Kaufman Assessment Battery for Children (Second Edition), attention using the Test of Variables of Attention, and motor skills using the Bruininks-Oseretsky Test of Motor Proficiency (Second Edition). Home environment was assessed using the Home Observation for the Measurement of the Environment (HOME). Age-adjusted test z-scores were entered into a regression model that adjusted for sex, socio-economic status score, HOME score, years of schooling, and ART treatment type.ResultsOne hundred and five children were tested; median (interquartile range) age was 7.05 years (6.30 to 8.44), CD4 count was 867.7 cells/mm3 (416.0 to 1203.5), and duration on ART was 4.03 years (3.55 to 4.23). Seventy-eight children had HIV subtype A and 27 had subtype D; the groups had comparable home and socio-economic status, except that there were more males among children infected with subtype A than D (64.7% vs. 35.3%, p = 0.02). There were no differences between the subtypes in general cognition (estimated mean difference: 0.20; 95% CI: -0.11 to 0.50); p = 0.21), attention (-0.18, 95% CI: -0.60 to 0.24, p = 0.41) and motor skills (1.60, 95% CI: -0.84 to 4.04, p = 0.20).ConclusionsOur results imply that ART may diminish the neurocognitive disadvantage seen in treatment-naïve HIV-infected children with subtype A.
Published: 2017

25. HIV Antibody Level as a Marker of HIV Persistence and Low-Level Viral Replication

Author: Keating, Sheila M, Pilcher, Christopher D, Jain, Vivek, Lebedeva, Mila, Hampton, Dylan, Abdel-Mohsen, Mohamed, Deng, Xutao, Murphy, Gary, Welte, Alex, Facente, Shelley N, Hecht, Frederick, Deeks, Steven G, Pillai, Satish K, and Busch, Michael P
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, HIV/AIDS, Biotechnology, Infectious Diseases, Infection, Antiretroviral Therapy, Highly Active, Biomarkers, Gene Expression Profiling, HIV Antibodies, HIV Antigens, HIV Infections, HIV-1, Humans, Longitudinal Studies, RNA, Viral, Specimen Handling, Viral Load, Virus Replication, Antibodies, HIV persistence, latent reservoir, incidence assay, Biological Sciences, Medical and Health Sciences, Microbiology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract: BackgroundHuman immunodeficiency virus (HIV) antibodies are generated and maintained by ongoing systemic expression of HIV antigen. We investigated whether HIV antibody responses as measured by high-throughput quantitative and qualitative assays could be used to indirectly measure persistent HIV replication in individuals receiving antiretroviral therapy (ART).MethodsHIV antibody responses were measured over time in the presence or absence of suppressive ART and were compared to the HIV reservoir size and expression of antiviral restriction factors.ResultsAmong untreated individuals, including both elite controllers (ie, persons with a viral load of ≤40 copies/mL) and noncontrollers, antibody parameters were stable over time and correlated with the individual viral load. Viral suppression with ART led to a progressive decline in antibody responses after treatment induction that persisted for 5-7 years. Higher levels of HIV antibodies during suppressive therapy were associated with later initiation of ART after infection, with higher DNA and cell-associated RNA levels, and with lower expression of multiple anti-HIV host restriction factors.DiscussionThese findings suggest that declining antibody levels during ART reflect lower levels of antigen production and/or viral replication in the persistent HIV reservoir. Results of relatively inexpensive and quantitative HIV antibody assays may be useful indirect markers that enable efficient monitoring of the viral reservoir and suppression during functional-cure interventions.
Published: 2017

26. Signature of the Sleeper Cell: A Biomarker of HIV Latency Revealed

Author: Pillai, Satish K and Deeks, Steven G
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, HIV/AIDS, Infectious Diseases, Infection, Biomarkers, CD4-Positive T-Lymphocytes, Gene Expression, HIV Infections, HIV-1, Humans, Molecular Targeted Therapy, RNA, Viral, Receptors, IgG, Virus Activation, Virus Latency, Biochemistry and cell biology
Abstract: HIV establishes a reservoir in latently infected T cells, and this reservoir has long hampered curative approaches. A recent study by Descours et al. identifies CD32a as a marker of latently infected T cells, potentially opening the way to the development of strategies that directly target this critical HIV reservoir.
Published: 2017

27. Short-Course Toll-Like Receptor 9 Agonist Treatment Impacts Innate Immunity and Plasma Viremia in Individuals With Human Immunodeficiency Virus Infection.

Author: Vibholm, Line, Schleimann, Mariane, Højen, Jesper, Benfield, Thomas, Offersen, Rasmus, Rasmussen, Katrine, Olesen, Rikke, Dige, Anders, Agnholt, Jørgen, Grau, Judith, Buzon, Maria, Wittig, Burghardt, Lichterfeld, Mathias, Petersen, Andreas, Deng, Xutao, Abdel-Mohsen, Mohamed, Pillai, Satish, Rutsaert, Sofie, Trypsteen, Wim, De Spiegelaere, Ward, Vandekerchove, Linos, Østergaard, Lars, Rasmussen, Thomas, Denton, Paul, Tolstrup, Martin, and Søgaard, Ole
Subjects: NK cell activation., TLR9 agonist, immune therapeutic treatment, latency reversal, latent HIV-1 infection, 2, 5-Oligoadenylate Synthetase, Antiretroviral Therapy, Highly Active, CD8-Positive T-Lymphocytes, Cytokines, DNA, Dendritic Cells, Female, HIV Infections, HIV-1, Humans, Immunity, Innate, Interferon-alpha, Killer Cells, Natural, Lymphocyte Activation, Male, Middle Aged, Myxovirus Resistance Proteins, RNA, Viral, Toll-Like Receptor 9, Ubiquitins, Viremia, Virus Latency
Abstract: BACKGROUND.: Treatment with latency reversing agents (LRAs) enhances human immunodeficiency virus type 1 (HIV-1) transcription in vivo but leads to only modest reductions in the size of the reservoir, possibly due to insufficient immune-mediated elimination of infected cells. We hypothesized that a single drug molecule-a novel Toll-like receptor 9 (TLR9) agonist, MGN1703-could function as an enhancer of innate immunity and an LRA in vivo. METHODS.: We conducted a single-arm, open-label study in which 15 virologically suppressed HIV-1-infected individuals on antiretroviral therapy received 60 mg MGN1703 subcutaneously twice weekly for 4 weeks. We characterized plasmacytoid dendritic cell, natural killer (NK), and T-cell activation using flow cytometry on baseline and after 4 weeks of treatment. HIV-1 transcription was quantified by measuring plasma HIV-1 RNA during MGN1703 administration. RESULTS.: In accordance with the cell type-specific expression of TLR9, MGN1703 treatment led to pronounced activation of plasmacytoid dendritic cells and substantial increases in plasma interferon-α2 levels (P < .0001). Consistently, transcription of interferon-stimulated genes (eg, OAS1, ISG15, Mx1; each P < .0001) were upregulated in CD4+ T cells as demonstrated by RNA sequencing. Further, proportions of activated cytotoxic NK cells and CD8+ T cells increased significantly during MGN1703 dosing, suggesting an enhancement of cellular immune responses. In 6 of 15 participants, plasma HIV-1 RNA increased from 1500 copies/mL (range, 21-1571 copies/mL) during treatment. CONCLUSIONS.: TLR9 agonist treatment in HIV infection has a dual potential by increasing HIV-1 transcription and enhancing cytotoxic NK cell activation, both of which are key outcomes in HIV-1 eradication therapy. CLINICAL TRIALS REGISTRATION.: NCT02443935.
Published: 2017

28. Identification and characterization of a rich population of CD34+ mesenchymal stem/stromal cells in human parotid, sublingual and submandibular glands.

Author: Togarrati, Padma Priya, Sasaki, Robson T, Abdel-Mohsen, Mohamed, Dinglasan, Nuntana, Deng, Xutao, Desai, Shivani, Emmerson, Elaine, Yee, Elizabeth, Ryan, William R, da Silva, Marcelo CP, Knox, Sarah M, Pillai, Satish K, and Muench, Marcus O
Subjects: Parotid Gland, Sublingual Gland, Submandibular Gland, Cells, Cultured, Mesenchymal Stem Cells, Animals, Humans, Mice, Antigens, CD34, Mesenchymal Stem Cell Transplantation, Signal Transduction, Cell Differentiation, Gene Expression Regulation, Adult, Middle Aged, Cells, Cultured, Antigens, CD34, Regenerative Medicine, Clinical Research, Digestive Diseases, Biotechnology, Stem Cell Research - Nonembryonic - Human, Transplantation, Stem Cell Research, Biochemistry and Cell Biology, Other Physical Sciences
Abstract: Mesenchymal stem/stromal cells (MSCs) play crucial roles in maintaining tissue homeostasis during physiological turnovers and injuries. Very little is known about the phenotype, distribution and molecular nature of MSCs in freshly isolated human salivary glands (SGs) as most reports have focused on the analysis of cultured MSCs. Our results demonstrate that the cell adhesion molecule CD34 was widely expressed by the MSCs of human major SGs, namely parotid (PAG), sublingual (SLG) and submandibular (SMG) glands. Further, gene expression analysis of CD34+ cells derived from fetal SMGs showed significant upregulation of genes involved in cellular adhesion, proliferation, branching, extracellular matrix remodeling and organ development. Moreover, CD34+ SMG cells exhibited elevated expression of genes encoding extracellular matrix, basement membrane proteins, and members of ERK, FGF and PDGF signaling pathways, which play key roles in glandular development, branching and homeostasis. In vitro CD34+ cell derived SG-MSCs revealed multilineage differentiation potential. Intraglandular transplantation of cultured MSCs in immunodeficient mice led to their engraftment in the injected and uninjected contralateral and ipsilateral glands. Engrafted cells could be localized to the stroma surrounding acini and ducts. In summary, our data show that CD34+ derived SG-MSCs could be a promising cell source for adoptive cell-based SG therapies, and bioengineering of artificial SGs.
Published: 2017

29. Cytokines Elevated in HIV Elite Controllers Reduce HIV Replication In Vitro and Modulate HIV Restriction Factor Expression

Author: Jacobs, Evan S, Keating, Sheila M, Abdel-Mohsen, Mohamed, Gibb, Stuart L, Heitman, John W, Inglis, Heather C, Martin, Jeffrey N, Zhang, Jinbing, Kaidarova, Zhanna, Deng, Xutao, Wu, Shiquan, Anastos, Kathryn, Crystal, Howard, Villacres, Maria C, Young, Mary, Greenblatt, Ruth M, Landay, Alan L, Gange, Stephen J, Deeks, Steven G, Golub, Elizabeth T, Pillai, Satish K, and Norris, Philip J
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, HIV/AIDS, Infectious Diseases, Clinical Research, Sexually Transmitted Infections, 2.1 Biological and endogenous factors, Infection, Adult, Antigens, Differentiation, CD4-Positive T-Lymphocytes, Cytokines, Female, Gene Expression Regulation, HIV, HIV Infections, HIV Long-Term Survivors, Humans, Membrane Proteins, Middle Aged, Plasma, Receptors, HIV, Virus Replication, chemokine receptors, cytokines, elite control, restriction factor, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract: A subset of HIV-infected individuals termed elite controllers (ECs) maintain CD4+ T cell counts and control viral replication in the absence of antiretroviral therapy (ART). Systemic cytokine responses may differentiate ECs from subjects with uncontrolled viral replication or from those who require ART to suppress viral replication. We measured 87 cytokines in four groups of women: 73 ECs, 42 with pharmacologically suppressed viremia (ART), 42 with uncontrolled viral replication (noncontrollers [NCs]), and 48 HIV-uninfected (NEG) subjects. Four cytokines were elevated in ECs but not NCs or ART subjects: CCL14, CCL21, CCL27, and XCL1. In addition, median stromal cell-derived factor-1 (SDF-1) levels were 43% higher in ECs than in NCs. The combination of the five cytokines suppressed R5 and X4 virus replication in resting CD4+ T cells, and individually SDF-1β, CCL14, and CCL27 suppressed R5 virus replication, while SDF-1β, CCL21, and CCL14 suppressed X4 virus replication. Functional studies revealed that the combination of the five cytokines upregulated CD69 and CCR5 and downregulated CXCR4 and CCR7 on CD4+ T cells. The CD69 and CXCR4 effects were driven by SDF-1, while CCL21 downregulated CCR7. The combination of the EC-associated cytokines induced expression of the anti-HIV host restriction factors IFITM1 and IFITM2 and suppressed expression of RNase L and SAMHD1. These results identify a set of cytokines that are elevated in ECs and define their effects on cellular activation, HIV coreceptor expression, and innate restriction factor expression. This cytokine pattern may be a signature characteristic of HIV-1 elite control, potentially important for HIV therapeutic and curative strategies.IMPORTANCE Approximately 1% of people infected with HIV control virus replication without taking antiviral medications. These subjects, termed elite controllers (ECs), are known to have stronger immune responses targeting HIV than the typical HIV-infected subject, but the exact mechanisms of how their immune responses control infection are not known. In this study, we identified five soluble immune signaling molecules (cytokines) in the blood that were higher in ECs than in subjects with typical chronic HIV infection. We demonstrated that these cytokines can activate CD4+ T cells, the target cells for HIV infection. Furthermore, these five EC-associated cytokines could change expression levels of intrinsic resistance factors, or molecules inside the target cell that fight HIV infection. This study is significant in that it identified cytokines elevated in subjects with a good immune response against HIV and defined potential mechanisms as to how these cytokines could induce resistance to the virus in target cells.
Published: 2017

30. Measuring the Size of the Latent Human Immunodeficiency Virus Reservoir: The Present and Future of Evaluating Eradication Strategies

Author: Henrich, Timothy J, Deeks, Steven G, and Pillai, Satish K
Subjects: Infectious Diseases, HIV/AIDS, Infection, Anti-HIV Agents, HIV, HIV Infections, Humans, Viral Load, Virus Latency, Human Immunodeficiency Virus, HIV reservoirs, HIV persistence, quantitative assays, antiretroviral treatment interruption, antiretroviral treatment interruption., Biological Sciences, Medical and Health Sciences, Microbiology
Abstract: One of the major barriers to the successful design and implementation of human immunodeficiency virus (HIV) curative strategies is the limited ability to sensitively, specifically, and precisely quantify and characterize the whole-body burden of replication-competent HIV in individuals on effective antiretroviral therapy. Here, we review the development and validation of assays that directly and indirectly measure the size and distribution of the reservoir in blood and tissues. We also discuss the role that treatment interruptions will have in validating these assays and ultimately as a "proof of cure."
Published: 2017

31. Population Movement Patterns Among the Democratic Republic of the Congo, Rwanda, and Uganda During an Outbreak of Ebola Virus Disease : Results from Community Engagement in Two Districts — Uganda, March 2019

Author: Nakiire, Lydia, Mwanja, Herman, Pillai, Satish K., Gasanani, Jonan, Ntungire, Dickson, Nsabiyumva, Stephen, Mafigiri, Richardson, Muneza, Nick, Ward, Sarah E., Daffe, Zeinabou, Ahabwe, Peter Babigumira, Kyazze, Simon, Ojwang, Joseph, Homsy, Jaco, Mclntyre, Elvira, Lamorde, Mohammed, Walwema, Richard, Makumbi, Issa, Muruta, Allan, and Merrill, Rebecca D.
Published: 2020

32. Human Galectin-9 Is a Potent Mediator of HIV Transcription and Reactivation.

Author: Abdel-Mohsen, Mohamed, Chavez, Leonard, Tandon, Ravi, Chew, Glen M, Deng, Xutao, Danesh, Ali, Keating, Sheila, Lanteri, Marion, Samuels, Michael L, Hoh, Rebecca, Sacha, Jonah B, Norris, Philip J, Niki, Toshiro, Shikuma, Cecilia M, Hirashima, Mitsuomi, Deeks, Steven G, Ndhlovu, Lishomwa C, and Pillai, Satish K
Subjects: CD4-Positive T-Lymphocytes, Humans, HIV-1, HIV Infections, Galectins, Anti-HIV Agents, Blotting, Western, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Gene Expression Profiling, Polymerase Chain Reaction, Virus Latency, Virus Activation, Transcription, Genetic, Transcriptome, Blotting, Western, Transcription, Genetic, Virology, Microbiology, Immunology, Medical Microbiology
Abstract: Identifying host immune determinants governing HIV transcription, latency and infectivity in vivo is critical to developing an HIV cure. Based on our recent finding that the host factor p21 regulates HIV transcription during antiretroviral therapy (ART), and published data demonstrating that the human carbohydrate-binding immunomodulatory protein galectin-9 regulates p21, we hypothesized that galectin-9 modulates HIV transcription. We report that the administration of a recombinant, stable form of galectin-9 (rGal-9) potently reverses HIV latency in vitro in the J-Lat HIV latency model. Furthermore, rGal-9 reverses HIV latency ex vivo in primary CD4+ T cells from HIV-infected, ART-suppressed individuals (p = 0.002), more potently than vorinostat (p = 0.02). rGal-9 co-administration with the latency reversal agent "JQ1", a bromodomain inhibitor, exhibits synergistic activity (p
Published: 2016

33. Investigation and Serologic Follow-Up of Contacts of Early Confirmed Case-Patient with COVID-19, Washington, USA

Author: Chu, Victoria T., Freeman-Ponder, Brandi, Lindquist, Scott, Spitters, Christopher, Kawakami, Vance, Dyal, Jonathan W., Clark, Shauna, Bruce, Hollianne, Duchin, Jeffrey S., DeBolt, Chas, Podczervinski, Sara, D'Angeli, Marisa, Pettrone, Kristen, Zacks, Rachael, Vahey, Grace, Holshue, Michelle L., Lang, Misty, Burke, Rachel M., Rolfes, Melissa A., Marlow, Mariel, Midgley, Claire M., Lu, Xiaoyan, Lindstrom, Stephen, Hall, Aron J., Fry, Alicia M., Thornburg, Natalie J., Gerber, Susan I., Pillai, Satish K., and Biggs, Holly M.
Subjects: Severe acute respiratory syndrome -- Health aspects, Enzyme-linked immunosorbent assay -- Health aspects, Coronaviruses -- Health aspects, Type 2 diabetes -- Health aspects, COVID-19 -- Health aspects, Health
Abstract: In December 2019, a viral pneumonia outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, China, before spreading rapidly to other provinces in China and then [...]
Published: 2020
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34. Modulation of Cellular Protein Trafficking by Human Immunodeficiency Virus Type 1 Nef: Role of the Acidic Residue in the ExxxLL Motif

Author: Madrid González, Ricardo, Coleman, Scott H., Van Damme, Nanette, Mitchell, Richard S., Bouchet, Jerome, Servant, Cecile, Pillai, Satish, Benichou, Serge, Guatelli, John C., Madrid González, Ricardo, Coleman, Scott H., Van Damme, Nanette, Mitchell, Richard S., Bouchet, Jerome, Servant, Cecile, Pillai, Satish, Benichou, Serge, and Guatelli, John C.
Abstract: The nef gene contributes to the replication of primate lentiviruses by altering the trafficking of cellular proteins involved in adaptive immunity (class I and II major histocompatibility complex [MHC]) and viral transmission (CD4 and DC-SIGN). A conserved acidic leucine-based sequence (E160xxxLL) within human immunodeficiency virus type 1 (HIV-1) Nef binds to the cellular adaptor protein (AP) complexes, which mediate protein sorting into endosomal vesicles. The leucine residues in this motif are required for the down-regulation of CD4 and for the up-regulation of DC-SIGN and the invariant chain of MHC class II, but the role of the acidic residue is unclear. Here, substitution of E160 with uncharged residues impaired the ability of Nef to up-regulate the expression of the invariant chain and DC-SIGN at the cell surface, whereas substitution with a basic residue was required for a similar effect on the down-regulation of CD4. All substitutions of E160 relieved the Nef-mediated block to transferrin uptake. E160 was required for the efficient interaction of Nef with AP-1 and AP-3 and for the stabilization of these complexes on endosomal membranes in living cells. Systematic mutation of the ExxxLL sequence together with correlation of binding and functional data leads to the hypotheses that AP-1 and AP-3 are major cofactors for the effect of Nef on the trafficking of transferrin, are less important but contribute to the modulation of the invariant chain and DC-SIGN, and are least critical for the modulation of CD4. The data suggest that the E160 residue plays a differential role in the modulation of leucine-dependent Nef-targets and support a model in which distinct AP complexes are used by Nef to modulate different cellular proteins., Depto. de Genética, Fisiología y Microbiología, Fac. de Ciencias Biológicas, TRUE, pub
Published: 2024

35. Select host restriction factors are associated with HIV persistence during antiretroviral therapy

Author: Abdel-Mohsen, Mohamed, Wang, Charlene, Strain, Matthew C, Lada, Steven M, Deng, Xutao, Cockerham, Leslie R, Pilcher, Christopher D, Hecht, Frederick M, Liegler, Teri, Richman, Douglas D, Deeks, Steven G, and Pillai, Satish K
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, Genetics, HIV/AIDS, Infectious Diseases, 2.1 Biological and endogenous factors, 2.2 Factors relating to the physical environment, 6.1 Pharmaceuticals, 5.1 Pharmaceuticals, Infection, Anti-HIV Agents, CD4-Positive T-Lymphocytes, HIV Infections, HIV-1, Host-Pathogen Interactions, Humans, Immunity, Cellular, Immunophenotyping, Lymphocyte Activation, RNA, Viral, Viral Load, Virus Latency, antiretroviral therapy, HIV latency, host restriction factors, intrinsic immunity, p21, PAF1 complex, schlafen 11, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology, Biomedical and clinical sciences, Health sciences
Abstract: ObjectiveThe eradication of HIV necessitates elimination of the HIV latent reservoir. Identifying host determinants governing latency and reservoir size in the setting of antiretroviral therapy (ART) is an important step in developing strategies to cure HIV infection. We sought to determine the impact of cell-intrinsic immunity on the HIV latent reservoir.DesignWe investigated the relevance of a comprehensive panel of established anti-HIV-1 host restriction factors to multiple established virologic and immunologic measures of viral persistence in HIV-1-infected, ART-suppressed individuals.MethodsWe measured the mRNA expression of 42 anti-HIV-1 host restriction factors, levels of cell-associated HIV-1 RNA, levels of total pol and 2-long terminal repeat (2-LTR) circle HIV-1 DNA and immunophenotypes of CD4 T cells in 72 HIV-1-infected individuals on suppressive ART (23 individuals initiated ART less than 1 year post-infection, and 49 individuals initiated ART greater than 1 year post-infection). Correlations were analysed using nonparametric tests.ResultsThe enhanced expression of a few select host restriction factors, p21, schlafen 11 and PAF1, was strongly associated with reduced CD4 T-cell associated HIV RNA during ART (P
Published: 2015

36. Dulaglutide and renal outcomes in type 2 diabetes: an exploratory analysis of the REWIND randomised, placebo-controlled trial

Author: Abella, Mercedes, Alebuena, Andrea, Almagro, Sandra, Amoroso, Eduardo, Anadon, Paula, Andreu, Elizabeth, Aristimuño, Guillermo, Arzadun, Maria, Barbieri, Maria, Barcudi, Raul, Bartolacci, Ines, Bolobanich, Gabriel, Bordonava, Anselmo, Bustamante Labarta, Miguel, Bustos, Betina, Caccavo, Alberto, Camino, Alejandra, Cantero, Maria, Carignano, Maria, Cartasegna, Luis, Cipullo, Marcela, Commendatore, Víctor, Conosciuto, Victoria, Costamagna, Osvaldo, Crespo, Claudia, Cuello, Jose, Cuneo, Carlos, Cusimano, Sandra, Dean, Sofia, Dituro, Claudio, Dominguez, Andrea, Farah, Miguel, Fernandez, Alberto, Fernandez, Florencia, Ferrari, Adriana, Flammia, Patricia, Fuentealba, Jose, Gallardo, Karina Beatriz, Garcia, Celso, Garcia Duran, Ruben, Garrido, Marcelo, Gavicola, Rodolfo, Gerbaudo, Claudio, Gilli, Graciela, Giotto, Ana Paula, Godoy Bolzán, Pedro, Gomez Vilamajo, Oscar, Guerlloy, Fernando, Guridi, Cristian, Gutierrez Garrido, Narcisa, Hasbani, Eduardo, Hermida, Sonia, Hominal, Miguel, Hrabar, Adrian, Ingaramo, Adrián, Izzicupo, Alejandra, Krynski, Mario, Lagrutta, Mariana, Lanchiotti, Paulina, Langhe, Maria, Leonard, Veronica, Llanos, Javier, Lopez Santi, Ricardo, Lowenstein, Jorge, Luquez, Cecilia, Mackinnon, Ignacio, Mana, Melina, Manzur, Sara, Marino, Javier, Martella, Carolina, Martinez, Roger, Matias, Re, Matkovich, Javier, Meritano, Monica, Montaña, Oscar, Mulazzi, María, Ochoa, Juan, Paterlini, Gustavo, Pelagagge, María, Peralta Lopez, Maria Elena, Prado, Aldo, Pruyas, Lorena, Racca, Martín, Ricotti, Carola, Rodriguez, Carolina, Romero Vidomlansky, Mariano, Ronderos, Ricardo, Sadowski, Ana Laura, Sala, Jorgelina, Sánchez, Alejandro, Santoro, Andrea, Schiavi, Lilia, Sein, Mariano, Sernia, Virginia, Serra, Leonardo, Sicer, Maximiliano, Smith, Tomas, Soso, Leonardo, Sposetti, Georgina, Steinacher, Andrea, Stival, Jorge, Tedesco, Jorge, Tonin, Hugo, Tortolo, Mauro, Ulla, Maria, Vallejos, Julio, Vico, Marisa, Virgillito, Luciana, Visco, Virginia, Vogel, Daniel, Waisman, Florencia, Zaidman, César, Zucchiatti, Noemi, Badshah, Imran, Cohen, Neale, Colman, Peter, Colquhoun, David, Davis, Timothy, Fourlanos, Spiros, Fulcher, Greg, Hamlyn, Jane, Haywood, Cilla, Hocking, Samantha, Huchinson, Maeve, Jeffries, William, Kyl, Mervyn, Lo, Clement, Mah, PeakMann, Makepeace, Ashley, Marope, Dolly, Nanayakkar, Natalie, Nankervis, Alison, Palmer, Neil, Palolus, Barbara, Pillai, Satish, Price, Sarah, Proietto, Joseph, Reutens, Anne, Rodrigo, Natassia, Sheikh, Abdul, Smith, Greg, So, Michelle, Soldatos, Georgia, Stuckey, Bronwyn, Sumithran, Priya, Teede, Helena, Vora, Parind, Williams, Lyn, Abib, Eduardo, Adão Poço, Christiani, Alves, Érica Ferreira, Andreatta Bernardi Barea, Janaina, Avezum Oliveira, Livia, Castro, Denise Ludovico da Costa de, Correa da Cruz, Ivan, Costa, Midiã, Cruz, Ivan, Cunha, Sidney, Da Silva, Marco Antonio Vieira, de Carvalho Camara Bona, Renata, de Paula, Bruna, Eliaschewitz, Freddy, Fazolli, Guilherme, Ferreira Filho, Carlos Alberto, Fortes, Jose, França, Cesar, Franco, Denise Reis, Genestreti, Paulo Roberto, Giorgeto, Flavio, Gonçalves, Rodrigo Marques, Grossman, Michele Elka, Henrique Marcelino, Ana Claudia, Hernandes, Mauro, Horta, Ana, Jaeger, Cristiano, Kaneblai, Midia, Kauffman Rutenberg, Cecilia, Kerr Saraiva, Jose Francisco, Lemos, Maria Angelica, Maia, Lilia, Manenti, Euler Roberto, Marques, Mariana, Melissa Valerio, Cynthia, Moreira, Rodrigo, Mothé, Flávia, Mouco, Osana Maria, Moura, Philip, Moura Jorge, José Carlos, Nakashima, Carlos, Nakazone, Marcelo, Napoli, Thiago, Nunes, Cristiane, Nunes Salles, Joao Eduardo, Oliveira, Karla, Oliveira, Marcela, Pantano, Gracielly de Souza, Petri, Fabio, Piazza, Leonardo, Pires, Andreia Carla, Pizzato, Patricia, Prata, Sergio, Precoma, Dalton, Rech, Rafael, Reis, Gilmar, Reis, Heleno, Resende, Elisabete, Ribas Fortes, Jose, Rodovalho, Sylka, Rossi dos Santos, Fabio, Salles, Joao Eduardo, Sampaio, Célia Regina, Santos, Thiago, Santos dos Santos, Vanessa, Silva e Quadros, Tulio, Silveira, Daniel, Siqueira, Katia Nunes, Teireira, M, Uehara, Marcelo, Valerio, C, Vianna, Henrique, Vidotti, Maria Helena, Visconti, Guilherme de Lima, Zanella, Maria Teresa, Andreeva, Viktoriya, Borisov, Radoslav, Botushanov, Nikolay, Dimitrov, Georgi, Dimova, Kameliya, Dragoychev, Tsvetan, Grigorova, Valentina, Gushterova, Valentina, Ivanov, Ivaylo, Kocelova, Tatyana, Kurktschiev, Dimo, Miletieva, Milena, Nenkova-Gugusheva, Neli, Pancheva, Ralitsa, Pavlova, Maria, Raev, Dimitar, Spasova, Vesela, Stoikov, Anastas, Troev, Dimitar, Yanev, Todor, Yoncheva-Mihaylova, Mariana, Abitbol, Alexander, Ajala, Buki, Alguwaihes, Abdullh, Ardilouze, Jean-Luc, Aris-Jilwan, Nahla, Arnaout, Amel, Aronson, Ronnie, Aslam, Nadeem, Babin, Sandra, Bailargeon, Jean-Patrice, Bailey, Allan, Bajaj, Harpreet, Beauchesne, Christian, Beca, Sorin, Belanger, Andre, Bell, Alan, Bellabarba, Diego, Berard, Lori, Berenbaum, Brian, Bergeron, Vincent, Berlingieri, Joseph, Bernier, Frédéric, Bishara, Phoebe, Blank, David, Blumer, Ian, Brault, Suzanne, Breton, Donald, Carpentier, André, Cha, James, Chandra, Prakash, Chiasson, Jean-Louis, Conway, James R, Couture, Ghyslaine, Couture, Nathalie, Dagenais, Gilles, Datta, Dyotirmoy, D'Ignazio, Giuseppe, Dumas, Richard, Fay, Didier, Frechette, Andre, Frenette, Louise, Fung, Daisy, Gagnon, Nathalie, Galter, Meri, Garon, Jean, Gauthier, Jean Sebastien, Geadah, Christian, Gilbert, Jeremy, Girard, Ronald, Goldenberg, Ronald, Grossman, Loren David, Gupta, Nikhil, Halle, Jean-Pierre, Hivert, Marie-France, Houde, Ghislaine, Houlden, Robyn, Hramiak, Irene, Jablonski, Ted, Jain, Akshay Jain, Khandwala, Hasnain, Khosla, Munish, Lachance, C, Laflamme, Emilie, Langlois, Marie-France, Larivee, Luc, Liutkus, Joanne, Lochnan, Heather, Malik, Saleem, McDonald, Charlotte, Mehta, Pravinsagar, Mihailidis, John, Milot, Alain, Narula, Priya, Nault, Patrice, Nayar, Arun, Nisker, William, Ouellet, Gilles, Palardy, Jean, Patel, Minta, Paul, Terri, Pedersen, Sue, Perron, Patrice, Pesant, Marie-Hélène, Poirier, Paul, Poulin, Marie-Claude, Punthakee, Zubin, Rehman, Waheed, Ross, Stuart, Sagar, P, Saliba, Nouhad, Sandler, Sam, Schiffrin, Alicia, Schlosser, Robert, Seth-Sharma, Anila, Sherman, Mark, Sionit, David, Sivakumar, Tharsan, Soto, Juan, St-Amour, Eric, Steen, Oren, Sussman, Jack, Telner, Adam, Tobe, Sheldon, Twum-Barima, David-Yaw, Van Zanten, Audrey, VanRossum, Nicole, Vecchiarelli, Jonathan, Ward, Rick, Wessengel, John, Weisnagel, Stanley, Wilderman, Igor, Woo, Vincent, Yakubovich, Natalia, Yale, Jean-Francois, Yared, Zeina, Acevedo, Monica, Aguirre, Maria Loreto, Aizman, Andres, Barroso, Maria Soledad, Cobos, Leonardo, Danin Vargas, Alfredo, Descalzi, Barbara, Godoy, Gonzalo, Grumberg, Elio, Lahsen, Rodolfo, Larenas, Gladys, Ortiz, Eugenia, Paredes, Javier, Potthoff, Sergio, Retamal, Eva, Rojas, Luis, Salgado, Manuel, Santibanez, Claudio, Solis, Carmen, Stokins, Benjamin, Accini, Jose, Acebedo, Javier, Agudelo Baena, Lina Maria, Alarcon, Soraya, Angel, Juliana, Arcos, Edgar, Aroca Martinez, M, Atuesta, Leonor, Balaguera, Jose, Ballestas, Doris, Barrera, Sandra Isabel, Barrios Reyes, Rosmy, Bayona, Adolfo, Bermudez, Andres, Bernal, Diego Zarate, Blanquicett, Marco, Bravo, Victor, Bueno, Wendy, Burbano Delgado, Alvaro, Cadena, Alberto, Cadena, Andres, Caicedo, Sandra, Celemin, Carlos, Consuegra, Ricardo, Contreras Pimienta, Cristhian, Corredor, Kelly Johenis, Cure, Carlos, De La Hoz Rueda, Lizeth Dayana, Delgado, Erika, Diaz, Sarahy, Diego, Marta, Donado, Anabell, Encinales Sanabria, William, Escobar, Juliana, Escorcia, Gillian, Forero, Leonardo, Fuentes, Laura, Garcia, Maria, Garcia Lozada, Henry, Garcia Ortiz, Luis, Giraldo, Angela, Gomez Gonzalez, Laura, Granada, Javier, Gutierrez, Corina, Henao, Natalia, Hernandez, Edwin, Herrera Uejbe, Olga Maria, Higuera Cobos, Juan Diego, Ibarra Gómez, Jaime, Jaimes, Edwin Hernandez, Jaramillo, Monica, Jaramillo, Nicolas, Jaramillo Gomez, Carlos, Jaramillo Sanchez, Monica, Jarava Durán, Ivonne, Lopez Ceballos, Catalina, Madrid, Claudia, María Amastha, Elias, Mercado, Jennifer, Molina, Dora Ines, Molina Soto, Jessica, Montoya, Carlos, Morales, Alexander, Muñoz, Carolina, Orozco, Luis Alejandro, Osorio, Oscar, Palmera Sanchez, Jorge Mario, Peña, Adwar, Perez, Jose, Perez Agudelo, Juan, Pérez Amador, Germán, Pertuz, Carlos, Posada, Irina, Puerta, Carlos, Quintero, Adalberto, Quiroz, Diana, Rendon, Carmen, Reyes, Alberto, Reyes, Alvaro, Ripoll, Diana, Rivera, Carlos, Rocha, Maria, Rodriguez, Jose F, Rodriguez Villanueva, Kervis Asid, Rodriguez Zabala, Javier Emilio, Rojas, Sindy, Romero, Maria, Rosero, Ricardo, Rosillo Cardenas, Angelica Rocio, Rueda, Lina, Sanchez, Gregorio, Sanchez, Tatiana, Sotomayor Herazo, Arístides, Suarez, Monica, Torres, Mariana, Trujillo, Freddy, Urina, Miguel, Van Strahlen, Lazaro, Velandia, Carlos, Velasquez Guzman, Carolina, Velazquez, Elizabeth, Vidal Prada, Tatiana, Yepez Alvaran, Juan Pablo, Zarate, Diego, Andelova, Jana, Benesova, Radka, Buzova, Barbara, Cech, Vladimir, Chodova, Ida, Choura, Miroslav, Dufka, Antonin, Gamova, Andrea, Gorgol, Jakub, Hala, Tomas, Havlova, Hana, Hlavkova, Dagmar, Horanska, Petra, Ilcisin-Valova, Juliana, Jenickova, Petra, Jerabek, Ondrej, Kantorova, Ilona, Kolomaznikova, Katerina, Kopeckova, Iva, Kopeckova, Miroslava, Linhart, Karel, Linhart, Tomas, Malecha, Jan, Malicherova, Emilia, Neubauerova, Dana, Oznerova, Martina, Partys, Radan, Pederzoliova, Eva, Petrusova, Maria, Prymkova, Vera, Racicka, Eva, Reissova, Ida, Roderova, Eva, Stanek, Libor, Striova, Alena, Svarcova, Dana, Svoboda, Petr, Szeghy Malicharova, Emilia, Urge, Jan, Vesely, Ladislav, Wasserburger, Bedich, Wasserburgerova, Hilde, Zahumensky, Emil, Zamrazil, Vaclav, Alawi, Hasan, Anastasiadis, Ernestos, Axthelm, Elisabeth, Bieler, Tasso, Buhrig, Christina, Degtyareva, Elizaveta, Dellanna, Frank, Derwahl, Karl-Michael, Diessel, Stephan, Dogiami, Barbara, Dorn-Weitzel, Kirsten, Ernst, Monika, Faulmann, Grit, Fetscher, Baerbel, Forst, Thomas, Freyer-Lahres, Gabriele, Funke, Klaus, Ganz, Xenia, Gleixner, Christiane, Hanefeld, Christoph, Heinrichs, Sven, Helleberg, Stephanie, Henkel, Elena, Hetzel, Gerd Ruediger, Hoffmann, Caren, Jacob, Frohmut, Jacob, Stephan, John, Franziska, Jonczyk, Antonius, Kamke, Wolfram, Klein, Christiane, Kleinhardt, Martina, Kleophas, Werner, Kosch, Christine, Kreutzmann, Kristin, Kühn, Achim, Lee-Barkey, Young Hee, Lier, Alexander, Maatouk, Sarah, Minnich, Joachim, Mitry, Michael, Muessig, Ilona, Nicula, Diana, Niemann, Martina, Nothroff, Joerg, Ott, Petra, Pfuetzner, Andreas, Pfützner, Andreas, Pistrosch, Frank, Pohl, Wildgard, Prochazkova, Zdenka, Retkowska, Marlena, Rosin, Heiko, Sachsenheimer, Daniela, Samer, Holger, Sanuri, Mazin, Schaefer, Axel, Schaper, Frank, Schulze, Erik-Delf, Schulze, Marita, Schumann, Martina, Segiet, Thomas, Sowa, Veronika, Stahl, Hans-Detlev, Steinfeldt, Franziska, Teige, Madlen, Trieb, Bjoern, Tschoepe, Diethelm, Uebel, Peter, Warken, Bernd, Weigmann, Ingo, Weyland, Klaus, Wilhelm, Klara, Balo, Timea, Balsay, Miklos, Bende, Ilona, Bezzegh, Katalin, Birkus, Zita, Buday, Barbara, Csomai, Melinda, Deak, Laszlo, Dezso, Eniko, Faludi, Peter, Faluvegi, M, Fazekas, Ilona, Feher, Agota, Fejer, Csaba, Finta, Ervin, Fulcz, Agnes, Gaal, Zsolt, Gurzo, Mihaly, Hati, Krisztina, Herczeg, Gabriella, Jozsef, Ildiko, Juhasz, Marta, Keltai, Katalin, Koranyi, Laszlo, Kulcsar, Eniko, Kun, Krisztina, Laczko, Andrea, Literáti-Nagy, Botond, Mezo, Izabella, Mileder, Margit, Moricz, I, Nagy, Károly, Nagybaczoni, Bela, Nemeth, Csaba, Oze, Agnes, Pauer, Jozsef, Peterfai, Eva, Polocsanyi, Bela, Poor, Ferenc, Reiber, István, Salamon, Csaba, Sebestyen, Julia, Torok, Ildiko, Tuu, Marianna, Varga, Andrea, Vass, Viktor, Ahn, Chul Min, Ahn, Chulwoo, ByungWon, Park, Chang, Hyuk-Jae, Chang, Kiyuk, Choi, Eui-Young, Choi, Han Seok, Chung, Jin-Wook, Hong, Bum- Kee, Hong, Young Joon, Hyon, Min Su, Jeong, Myung Ho, Kang, Shinae, Kim, Byeong-Keuk, Kim, Ji-Hyun, Kim, Ju Han, Kim, Kee-Sik, Kim, Moo Hyun, Kim, Pum-Joon, Kim, Soon-Kil, Kim, Yong-Seok, Kim, Young Kwon, Koh, Yoon Seok, Kwon, Hyuck Moon, Lee, Byoung Kwon, Lee, Byung-Wan, Lee, Jin Bae, Lee, Myoung-Mook, Lim, Young-Mee, Min, Pil Ki, Park, Jong Sung, Park, Jongsuk, Park, Keun Ho, Park, Sungha, Pyun, Wook Bum, Rim, Se Joong, Ryu, Dong-Ryeol, Seo, Hong-Seog, Seung, Ki Bae, Shin, Dong-Ho, Sim, Doo Sun, Yoon, Young Won, Andersone, Ilze, Babicka, Kristine, Balcere, Inga, Barons, Roberts, Capkovska, Inguna, Geldnere, Kristine, Grigane, Inese, Jegere, Baiba, Lagzdina, Ilze, Mora, Lija, Pastare, Sigita, Ritenberga, Rota, Romanova, Janina, Saknite, Inta, Sidlovska, Natalja, Sokolova, Jelena, Steina, Sandra, Strizko, Iveta, Teterovska, Dace, Vizina, Brigita, Barsiene, Lina, Belozariene, Gintare, Daugintyte-Petrusiene, Laura, Drungiliene, Nijole, Garsviene, Nijole, Grigiene, Ala, Grizas, Vytautas, Jociene, Virginija, Kalvaitiene, Dalia, Kaupiene, Jugeta, Kavaliauskiene, Jurate, Kozloviene, Dalia, Lapteva, Ilona, Maneikiene, Birute, Marcinkeviciene, Jolanta, Markauskiene, Vaidilija, Meiluniene, Salomeja, Norkus, Almantas, Norviliene, Rita, Petrenko, Vladimiras, Radzeviciene, Ruta, Sakalyte, Gintare, Urbonas, Gediminas, Urbutiene, Skaiste, Vasiliauskas, Donatas, Velickiene, Dzilda, Aguilar, Carlos, Alcocer, Marco, Avalos-Ramirez, Juan Antonio, Banda-Elizondo, Ramiro, Bricio-Ramirez, Rubria, Cardenas Mejia, Karla, Cavazos, Francisco, Chapa, Jesus, Cienfuegos, Erika, De la Peña, Astrid, de la Peña Topete, Gilberto, De los Rios Ibarra, Manuel Odin, Elias, Daniel, Flores-Moreno, Claudia, Garcia Hernandez, Pedro, Gonzalez, Luis Gerardo, Guerra Moya, Rosa Linda, Guerra-Lopez, Arturo, Hernandez Baylon, Raymundo, Herrera Colorado, Carolina, Herrera-Marmolejo, Marisol, Islas-Palacios, Neri, Lopez, Esteban, Lopez, Fernando, Lopez Alvarado, Agustin, Luna Ceballos, Rosa Isela, Morales Villegas, Enrique, Moreno-Virgen, Gualberto, Parra Perez, Rosa Linda, Pascoe Gonzalez, Sara, Peralta-Cantu, Irving, Previn, Roopa, Ramirez, Rosa, Ramirez, Rubria, Ramos Zavala, Maria Guadalupe, Rodriguez, Monica, Salgado-Sedano, Rocio, Sanchez-Aguilar, Ana Claudia, Santa Rosa Franco, Edith, Sauque-Reyna, Leobardo, Suarez Otero, Rodrigo, Torres, Ivonne, Velarde-Harnandez, Enrique, Villagordoa, Juan, Villeda-Espinoza, Efrain, Vital-Lopez, Jorge, Zavala- Bello, Cristian Jair, Baker, John, Barrington-Ward, Elaine, Brownless, Thomas, Carroll, Richard, Carson, Simon, Choe, Michelle, Corin, Andrew, Corley, Brian, Cutfield, Richard, Dalaman, Neelam, Dixon, Paul, Drury, Paul, Dyson, Keith, Florkowski, Chris, Ford, Monica, Frengley, William, Helm, Colin, Katzen, Colin, Kerr, Jane, Khanolkar, Manish, Kim, David, Koops, Renata, Krebs, Jeremy, Leikis, Robert, Low, Kwan, Luckey, Alison, Luke, Richard, Macaulay, Susan, Marks, Rodney, McNamara, Catherine, Millar-Coote, Dean, Miller, Steven, Mottershead, Naomi, Reid, James, Robertson, Narcisa, Rosen, Ian, Rowe, David, Schmiedel, Ole, Scott, Russell, Sebastian, Jeffrey, Sheahan, Davitt, Stiebel, Victoria, Ternouth, Ian, Tofield, Chris, Venter, Dirk, Williams, Michael, Williams, Miles, Wu, Fiona, Young, Simon, Arciszewska, Malgorzata, Bochenek, Anna, Borkowski, Piotr, Borowy, Przemyslaw, Chrzanowski, Tomasz, Czerwinski, Edward, Dwojak, Marek, Grodzicka, Agnieszka, Janiec, Izabela, Jaruga, Joanna, Jazwinska-Tarnawska, Ewa Krystyna, Jedynasty, Krystyna, Juzwiak-Czapiewska, Danuta, Karczewicz-Janowska, Jadwiga, Konieczny, Jan, Konieczny, Marek, Korol, Marek, Kozina, Maciej, Krzyzagorska, Ewa, Kucharczyk-Petryka, Ewa, Laz, Roman, Majchrzak, Anna, Mrozowska, Zdzislawa, Mularczyk, Michal, Nowacka, Elzbieta, Peczynska, Jadwiga, Petryka, Robert, Pietrzak, Radoslaw, Pisarczyk-Wiza, Dorota, Rozanska, Aleksandra, Ruzga, Zofia, Rzeszotarska, Emilia, Sacha, Malgorzata, Sekulska, Marzenna, Sidorowicz-Bialynicka, Anna, Stasinska, Teresa, Strzelecka-Sosik, Agnieszka, Swierszcz, Teresa, Szymkowiak, Katarzyna Miroslawa, Turowska, Olga, Wisniewska, Krystyna, Wiza, Maciej, Wozniak, Iwona, Zelazowska, Katarzyna, Ziolkowska-Gawron, Bernadetta, Zytkiewicz-Jaruga, Danuta, Albota, Adrian, Alexandru, Carmina, Avram, Rodica, Bala, Cornelia, Barbonta, Diana, Barbu, Roxana, Braicu, Daniela, Calutiu, Nicoleta, Catrinoiu, Doina, Cerghizan, Anca, Ciorba, Alina, Craciun, Anca, Doros, Rodica, Duma, Livia, Dumitrache, Ancuta, Ferariu, Ioana, Ferician Moza, Anca, Ghergan, Alexandrina, Ghise, Gheorghe, Graur, Mariana, Gribovschi, Mihaela, Mihai, Bogdan, Mihalache, Laura, Mihalcea, Madalina, Mindrescu, Nicoleta, Morosanu, Magdalena, Morosoanu, Andrea, Mota, Maria, Moza, Anca, Nafornita, Valerica, Natea, Narcisa, Nicodim, Simona, Nita, Cristina, Onaca, Adriana, Onaca, Mircea, Pop, Cristina, Pop, Lavinia, Popa, Amorin, Popescu, Alexandrina, Pruna, Luchiana, Roman, Gabriela, Rosu, Mihaela, Sima, Alexandra, Sipciu, Doina, Sitterli-Natea, Carmen Narcisa, Szilagyi, Iosif, Tapurica, Minodora, Tase, Adrian, Tutescu, Adriana-Carmen, Vanghelie, Luminita, Verde, Ioana, Vlad, Adrian, Zarnescu, Mihaela, Akhmetov, Roman, Allenova, Irina, Avdeeva, Irina, Baturina, Oksana, Biserova, Irina, Bokovin, Nikolay, Bondar, Irina, Burova, Natalia, Chufeneva, Galina, Chumachek, Elena, Demidova, Marina, Demin, Alexander, Drobysheva, Vera, Egorova, Irina, Esenyan, Lev, Gelig, Ekaterina, Gilyarevsky, Sergey, Golshmid, Maria, Goncharov, Arseniy, Gorbunova, Anastasia, Gordeev, Ivan, Gorelysheva, Vera, Goryunova, Tatiana, Grebenshchikova, Irina, Ilchenko, Roman, Ivannikova, Maria, Karabalieva, Saule, Karpeeva, Juliya, Khaykina, Elena, Kobalava, Zhanna, Kononenko, Irina, Korolik, Oxana, Korshunova, Anna, Kostenko, Victor, Krasnopevtseva, Irina, Krylova, Ludmila, Kulkova, Polina, Kuzmina, Irina, Ledyaeva, Alla, Levashov, Sergey, Lokhovinina, Natalia, Lvov, Vadim, Martirosyan, Narine, Nedogoda, Sergey, Nilk, Rostislav, Osmolovskaya, Yulia, Panov, Alexey, Paramonova, Olga, Pavlova, Ekaterina, Pekareva, Elena, Petunina, Nina, Ponamareva, Svetlana, Reshedko, Galina, Salasyuk, Alla, Sepkhanyan, Malvina, Serebrov, Alexandr, Shabelnikova, Olesya, Skvortsov, Andrey, Smirnova, Olga, Spiridonova, Oxana, Strogova, Svetlana, Taratukhin, Evgeny, Tereschenko, Sergey, Trukhina, Lubov, Tsarkova, Olga, Tsoma, Vera, Tumarov, Farid, Tyan, Natalya, Tyurina, Tatiana, Villevalde, Svetlana, Yankovaya, Elena, Zarutskaya, Ludmila, Zenkova, Elena, Badat, Aysha, Bester, Frederik, Blignaut, Suzanne, Blom, Dirk, Booysen, Susan, Boyd, Warren, Brice, Brigitte, Brown, Susan, Burgess, Lesley, Cawood, Reina, Coetzee, Kathleen, Conradie, Hillet, Cronje, Tanja, de Jong, Douwe, Ellis, Graham, Emanuel, Shaunagh, Engelbrecht, Ingrid, Foulkes, Sharne, Fourie, Done, Gibson, Gilbert, Govender, Thirumani, Hansa, Sumayah, Hemus, Allana Colleen, Hendricks, Firzana, Heradien, Marshall, Holmgren, Chantelle, Hoosain, Zaheer, Horak, Emile, Howard, Johannes, Immink, Ignatius, Janari, E., Jivan, Daksha, Klusmann, Karl, Labuschagne, Weik, Lai, Yen-yu, Latiff, Gulam, Lombaard, J., Lottering, Hanlie, Meeding, Ronel, Middlemost, Shirley, Mitha, Haroon, Mitha, Ismail, Mkhwanazi, Sandile, Moodley, Rajendran, Murray, Almeri, Musungaie, Dany, Osman, Yasmin, Peacey, Kirsten, Pillay-Ramaya, Larisha, Pretorius, Catharina, Prozesky, Hans, Sarvan, Mahomed, Scholtz, E, Sebesteny, Attila, Skinner, Bianca, Skriker, Michael, Smit, M, Stapelberg, Anna-Marie, Swanepoel, Nicolaas, Urbach, Dorothea, van Aswegen, Dina, van Zyl, Francois, Van Zyl, Louis, Venter, Esme, Wadvalla, Shahid, Wing, Jeffrey, Wolmarans, Karen, Abreu, Cristina, Aguilà, Pilar, Aguilera, Eva, Alonso, Nuria, Alvarez, Carmen, Cajas, Priscila, Castro, Jose Carlos, Codinachs, Roger, Contreras, Jose, Coves, Maria Jose, Fajardo, Carmen, Ferrer, Juan Carlos, Font, Neus, Garcia, Mar, Gil, Maria Apolonia, Gomez, Fernando, Gomez, Lluis Alberto, Gonzalbez, Jose, Griera, Jose Luis, Masmiquel, Luís, Mauricio, Didac, Narejos Perez, Silvia, Nicolau, Juana Ana, Noheda Contreras, Olga, Olivan, Josefina, Olivares, Josefina, Ortega, Emilio, Pellitero, Silvia, Pertusa, Salvador, Rius, Ferran, Rodriguez, Irene, Sánchez-Juan, Carlos, Santos, Dolores, Soldevila, Berta, Subias, David, Terns, Manel, Trescoli, Carlos, Vilaplana, Judith, Villanueva, Alicia, Albo, Jaan, Antus, Kjell, Axelsson, Mattias, Bergström, Lisa, Binsell-Gerdin, Emil, Boman, Kurt, Botond, Fabian, Dotevall, Annika, Graipe, Anna, Jarnet, C, Kaminska, Jessica, Kempe, Anders, Korhonen, Michael, Linderfalk, Carina, Liu, Bo, Ljungstroem, Karl, Ljungström, Karl, Malmqvist, Lennart, Mellbin, Linda, Mooe, Thomas, Nicol, Peter, Norrby, Anders, Ohlsson, Ake, Rosengren, Annika, Saaf, Jan, Salmonsson, Staffan, Strandberg, Olof, Svensson, Karl-Axel, Tengmark, Bengt-Olov, Tsatsaris, Georgios, Ulvenstam, Anders, Vasko, Peter, Chang, Chwen-Tzuei, Chang, Hsin-Mei, Chen, Jung-Fu, Chen, To-Pang, Chung, Ming-Min, Fu, Chia-Po, Hsia, Te-Lin, Hua, Shih-Che, Kuo, Ming-Chun, Lee, Chia-ln, Lee, I-Te, Liang, Kae-Woei, Lin, Shih Yi, Lu, Chieh-Hsiang, Ma, Wen-Ya, Pei, Dee, Shen, Feng-Chih, Su, Ching-Chieh, Su, Shuo-Wei, Tai, Tsai-Sung, Tsai, Wan-Ni, Tsai, Yi-Ting, Tung, Shih-Chen, Wang, Jun-Sing, Yu, Hui-I, Al-Qaissi, Ahmed, Arutchelvam, Vijayaraman, Atkin, Stephen, Au, Simon, Aye, Myint Myint, Bain, Stephen, Bejnariu, Cristina, Bell, Patrick, Bhatnagar, Deepak, Bilous, Rudy, Black, Neil, Brennan, Ursula, Brett, Barbara, Bujanova, Jana, Chow, Elaine, Collier, Andrew, Combe, Amanda, Courtney, Christopher, Courtney, Hamish, Crothers, James, Eavis, Patrick, Elliott, Jackie, Febbraro, Salvatore, Finlayson, Jim, Gandhi, Rajiv, Gillings, Sharon, Hamling, Jonathan, Harper, Roy, Harris, Tim, Hassan, Kahal, Heller, Simon, Jane, Alison, Javed, Zeeshan, Johnson, Tim, Jones, Stephen, Kennedy, Adele, Kerr, David, Kilgallon, Brian, Konya, Judith, Lindsay, John, Lomova-Williams, Lina, Looker, Helen, MacFarlane, David, Macrury, Sandra, Malik, Iqbal, McCrimmon, Rory, McKeith, Douglas, McKnight, John, Mishra, Biswa, Mukhtar, Racha, Mulligan, Ciara, O'Kane, Maurice, Olateju, Tolu, Orpen, Ian, Richardson, Tristan, Rooney, Desmond, Ross, Shorsha Bae, Sathyapalan, Thozhukat, Siddaramaiah, Naveen, Sit, Lee Euan, Stephens, Jeffrey, Turtle, Frances, Wakil, Ammar, Walkinshaw, Emma, Ali, Asem, Anderson, Robert, Arakaki, Richard, Aref, Omar, Ariani, Mehrdad Kevin, Arkin, David, Banarer, Salomon, Barchini, George, Bhan, Arti, Branch, Kelley, Brautigam, Donald, Brietzke, Stephen, Brinas, Maridez, Brito, Yudit, Carter, Casey, Casagni, Kimberely, Casula, Sabina, Chakko, Simon, Charatz, Seth, Childress, Dale, Chow, Lisa, Chustecka, Malgorzata, Clarke, Subha, Cohen, Lisa, Collins, Barry, Colon Vega, Gildred, Comulada-Rivera, Angel, Cortes-Maisonet, Gregorio, Davis, Matthew, de Souza, Jose, Desouza, Cyrus, Dinnan, Mary, Duffy-Hidalgo, Bobbi, Dunn, Barbara, Dunn, Julia, Elman, Marshall, Felicetta, James, Finkelstein, Stuart, Fitz-Patrick, David, Florez, Hermes, Forker, Alan, Fowler, Wayne, Fredrickson, Sonja, Freedman, Zachary, Gainey Narron, Brooke, Gainey-Ferree, Kristin, Gardner, Michael, Gastelum, Christian, Giddings, Stephen, Gillespie, Eve, Gimness, Michael Paul, Goldstein, Gary, Gomes, Maria, Gomez, Nelson, Gorman, Timothy, Goswami, Ketan, Graves, Arthur, Hacking, Scott, Hall, Charles, Hanson, Lenita, Harman, Sherman, Heber, David, Henry, Robert, Hiner, Janette, Hirsch, Irl, Hollander, Priscilla, Hooker, Thomas, Horowitz, Barry, Hoste, Laura, Huang, Loli, Huynh, Minh, Hyman, Dan, Idriss, Soha, Iranmanesh, Ali, Karounos, Dennis, Kashyap, Moti, Katz, Lois, Kaye, William, Khaiton, Yevgeniy, Khardori, Romesh, Kitchen, Timothy, Klein, Andrew, Knffem, Wendi, Kosiborod, Mikhail, Kreglinger, Nicola, Kruger, Davida, Kumar, Anubhav, Laboy, Ivan, Larrabee, Patricia, Larrick, Laura, Lawson, Donna, Ledet, Mike, Lenhard, James, Levy, James, Li, George, Li, Zhaoping, Lieb, David, Limcolioc, April, Lions-Patterson, Jane, Lorber, Daniel, Lorch, Daniel, Lorrello, Michael, Lu, Peter, Lucas, Kathryn Jean, Ma, Siu-Ling, MacAdams, Michael, Magee, Michelle, Magno, Alexander, Mahakala, Aparna Reddy, Marks, Jennifer, McCall, Anthony, McClanahan, William, Jr., McClary, Carole, Melendez, Lydia, Melish, John, Michaud, Deanna, Miller, Christopher, Miller, Neil, Mora, Pablo, Moten, Marriyam, Mudaliar, Sunder, Myrick, Gregory, Narayan, Puneet, Nassif, Mike, Neri, Karena, Newton, Tabitha, Niblack, Patricia, Nicol, Philip, Nyenwe, Ebenezer, Odugbesan, A. Ola, Okorocha, Yolanda, Ortiz Carrasquillo, Ramón, Osei, Kwame, Palermo, Coromoto, Patel, Hiren, Patel, Krishna, Pau, Cindy, Perley, Michael, Plevin, Sanford, Plummer, Elena, Powell, Richard, Qintar, Mohammed, Rawls, Rex, Reyes-Castano, John, Reynolds, Lillian, Richards, Robert, Rosenstock, Julio, Rowe, Caroline, Saleh, Jahandar, Sam, Sony, Sanchez, Alfredo, Sander, Donald, Sanderson, Bruce, Savin, Virginia, Seaquist, Elizabeth, Shah, Jayendra, Shi, Serena, Shivaswamy, Vijay, Shlotzhauer, Tammi, Shore, David, Skukowski, Bobbie, Soe, Kyaw, Solheim, Vesna, Soufer, Joseph, Steinberg, Helmut, Steinsapir, Jaime, Tarkington, Phillip, Thayer, Debra, Thomson, Stephen, Thrasher, James, Tibaldi, Joseph, Tjaden, Jeff, Tores, Oberto, Trence, Dace, Trikudanathan, Subbulaxmi, Ullal, Jagdeesh, Uwaifo, Gabriel, Vo, Anthony, Vu, Kenny, Walia, Damandeep, Weiland, Karen, Whitehouse, Fred, Wiegmann, Thomas, Wyne, Kathleen, Wynne, Alan, Yuen, Kevin, Zaretzky, Joel, Zebrack, James, Zieve, Franklin, Zigrang, William, Gerstein, Hertzel C, Colhoun, Helen M, Dagenais, Gilles R, Diaz, Rafael, Lakshmanan, Mark, Pais, Prem, Probstfield, Jeffrey, Botros, Fady T, Riddle, Matthew C, Rydén, Lars, Xavier, Denis, Atisso, Charles Messan, Dyal, Leanne, Hall, Stephanie, Rao-Melacini, Purnima, Wong, Gloria, Avezum, Alvaro, Basile, Jan, Chung, Namsik, Conget, Ignacio, Cushman, William C, Franek, Edward, Hancu, Nicolae, Hanefeld, Markolf, Holt, Shaun, Jansky, Petr, Keltai, Matyas, Lanas, Fernando, Leiter, Lawrence A, Lopez-Jaramillo, Patricio, Cardona Munoz, Ernesto German, Pirags, Valdis, Pogosova, Nana, Raubenheimer, Peter J, Shaw, Jonathan E, Sheu, Wayne H-H, and Temelkova-Kurktschiev, Theodora
Published: 2019
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37. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial

Author: Abella, Mercedes, Alebuena, Andrea, Almagro, Sandra, Amoroso, Eduardo, Anadon, Paula, Andreu, Elizabeth, Aristimuño, Guillermo, Arzadun, Maria, Barbieri, Maria, Barcudi, Raul, Bartolacci, Ines, Bolobanich, Gabriel, Bordonava, Anselmo, Bustamante Labarta, Miguel, Bustos, Betina, Caccavo, Alberto, Camino, Alejandra, Cantero, Maria, Carignano, Maria, Cartasegna, Luis, Cipullo, Marcela, Commendatore, Víctor, Conosciuto, Victoria, Costamagna, Osvaldo, Crespo, Claudia, Cuello, Jose, Cuneo, Carlos, Cusimano, Sandra, Dean, Sofia, Dituro, Claudio, Dominguez, Andrea, Farah, Miguel, Fernandez, Alberto, Fernandez, Florencia, Ferrari, Adriana, Flammia, Patricia, Fuentealba, Jose, Gallardo, Karina Beatriz, Garcia, Celso, Garcia Duran, Ruben, Garrido, Marcelo, Gavicola, Rodolfo, Gerbaudo, Claudio, Gilli, Graciela, Giotto, Ana Paula, Godoy Bolzán, Pedro, Gomez Vilamajo, Oscar, Guerlloy, Fernando, Guridi, Cristian, Gutierrez Garrido, Narcisa, Hasbani, Eduardo, Hermida, Sonia, Hominal, Miguel, Hrabar, Adrian, Ingaramo, Adrián, Izzicupo, Alejandra, Krynski, Mario, Lagrutta, Mariana, Lanchiotti, Paulina, Langhe, Maria, Leonard, Veronica, Llanos, Javier, Lopez Santi, Ricardo, Lowenstein, Jorge, Luquez, Cecilia, Mackinnon, Ignacio, Mana, Melina, Manzur, Sara, Marino, Javier, Martella, Carolina, Martinez, Roger, Matias, Re, Matkovich, Javier, Meritano, Monica, Montaña, Oscar, Mulazzi, María, Ochoa, Juan, Paterlini, Gustavo, Pelagagge, María, Peralta Lopez, Maria Elena, Prado, Aldo, Pruyas, Lorena, Racca, Martín, Ricotti, Carola, Rodriguez, Carolina, Romero Vidomlansky, Mariano, Ronderos, Ricardo, Sadowski, Ana Laura, Sala, Jorgelina, Sánchez, Alejandro, Santoro, Andrea, Schiavi, Lilia, Sein, Mariano, Sernia, Virginia, Serra, Leonardo, Sicer, Maximiliano, Smith, Tomas, Soso, Leonardo, Sposetti, Georgina, Steinacher, Andrea, Stival, Jorge, Tedesco, Jorge, Tonin, Hugo, Tortolo, Mauro, Ulla, Maria, Vallejos, Julio, Vico, Marisa, Virgillito, Luciana, Visco, Virginia, Vogel, Daniel, Waisman, Florencia, Zaidman, César, Zucchiatti, Noemi, Badshah, Imran, Cohen, Neale, Colman, Peter, Colquhoun, David, Davis, Timothy, Fourlanos, Spiros, Fulcher, Greg, Hamlyn, Jane, Haywood, Cilla, Hocking, Samantha, Huchinson, Maeve, Jeffries, William, Kyl, Mervyn, Lo, Clement, Mah, PeakMann, Makepeace, Ashley, Marope, Dolly, Nanayakkar, Natalie, Nankervis, Alison, Palmer, Neil, Palolus, Barbara, Pillai, Satish, Price, Sarah, Proietto, Joseph, Reutens, Anne, Rodrigo, Natassia, Sheikh, Abdul, Smith, Greg, So, Michelle, Soldatos, Georgia, Stuckey, Bronwyn, Sumithran, Priya, Teede, Helena, Vora, Parind, Williams, Lyn, Abib, Eduardo, Adão Poço, Christiani, Alves, Érica Ferreira, Andreatta Bernardi Barea, Janaina, Avezum Oliveira, Livia, Castro, Denise Ludovico da Costa de, Correa da Cruz, Ivan, Costa, Midiã, Cruz, Ivan, Cunha, Sidney, Da Silva, Marco Antonio Vieira, de Carvalho Camara Bona, Renata, de Paula, Bruna, Eliaschewitz, Freddy, Fazolli, Guilherme, Ferreira Filho, Carlos Alberto, Fortes, Jose, França, Cesar, Franco, Denise Reis, Genestreti, Paulo Roberto, Giorgeto, Flavio, Gonçalves, Rodrigo Marques, Grossman, Michele Elka, Henrique Marcelino, Ana Claudia, Hernandes, Mauro, Horta, Ana, Jaeger, Cristiano, Kaneblai, Midia, Kauffman Rutenberg, Cecilia, Kerr Saraiva, Jose Francisco, Lemos, Maria Angelica, Maia, Lilia, Manenti, Euler Roberto, Marques, Mariana, Melissa Valerio, Cynthia, Moreira, Rodrigo, Mothé, Flávia, Mouco, Osana Maria, Moura, Philip, Moura Jorge, José Carlos, Nakashima, Carlos, Nakazone, Marcelo, Napoli, Thiago, Nunes, Cristiane, Nunes Salles, Joao Eduardo, Oliveira, Karla, Oliveira, Marcela, Pantano, Gracielly de Souza, Petri, Fabio, Piazza, Leonardo, Pires, Andreia Carla, Pizzato, Patricia, Prata, Sergio, Precoma, Dalton, Rech, Rafael, Reis, Gilmar, Reis, Heleno, Resende, Elisabete, Ribas Fortes, Jose, Rodovalho, Sylka, Rossi dos Santos, Fabio, Salles, Joao Eduardo, Sampaio, Célia Regina, Santos, Thiago, Santos dos Santos, Vanessa, Silva e Quadros, Tulio, Silveira, Daniel, Siqueira, Katia Nunes, Teireira, M, Uehara, Marcelo, Valerio, C, Vianna, Henrique, Vidotti, Maria Helena, Visconti, Guilherme de Lima, Zanella, Maria Teresa, Andreeva, Viktoriya, Borisov, Radoslav, Botushanov, Nikolay, Dimitrov, Georgi, Dimova, Kameliya, Dragoychev, Tsvetan, Grigorova, Valentina, Gushterova, Valentina, Ivanov, Ivaylo, Kocelova, Tatyana, Kurktschiev, Dimo, Miletieva, Milena, Nenkova-Gugusheva, Neli, Pancheva, Ralitsa, Pavlova, Maria, Raev, Dimitar, Spasova, Vesela, Stoikov, Anastas, Troev, Dimitar, Yanev, Todor, Yoncheva-Mihaylova, Mariana, Abitbol, Alexander, Ajala, Buki, Alguwaihes, Abdullh, Ardilouze, Jean-Luc, Aris-Jilwan, Nahla, Arnaout, Amel, Aronson, Ronnie, Aslam, Nadeem, Babin, Sandra, Bailargeon, Jean-Patrice, Bailey, Allan, Bajaj, Harpreet, Beauchesne, Christian, Beca, Sorin, Belanger, Andre, Bell, Alan, Bellabarba, Diego, Berard, Lori, Berenbaum, Brian, Bergeron, Vincent, Berlingieri, Joseph, Bernier, Frédéric, Bishara, Phoebe, Blank, David, Blumer, Ian, Brault, Suzanne, Breton, Donald, Carpentier, André, Cha, James, Chandra, Prakash, Chiasson, Jean-Louis, Conway, James R, Couture, Ghyslaine, Couture, Nathalie, Dagenais, Gilles, Datta, Dyotirmoy, D'Ignazio, Giuseppe, Dumas, Richard, Fay, Didier, Frechette, Andre, Frenette, Louise, Fung, Daisy, Gagnon, Nathalie, Galter, Meri, Garon, Jean, Gauthier, Jean Sebastien, Geadah, Christian, Gilbert, Jeremy, Girard, Ronald, Goldenberg, Ronald, Grossman, Loren David, Gupta, Nikhil, Halle, Jean-Pierre, Hivert, Marie-France, Houde, Ghislaine, Houlden, Robyn, Hramiak, Irene, Jablonski, Ted, Jain, Akshay Jain, Khandwala, Hasnain, Khosla, Munish, Lachance, C, Laflamme, Emilie, Langlois, Marie-France, Larivee, Luc, Liutkus, Joanne, Lochnan, Heather, Malik, Saleem, McDonald, Charlotte, Mehta, Pravinsagar, Mihailidis, John, Milot, Alain, Narula, Priya, Nault, Patrice, Nayar, Arun, Nisker, William, Ouellet, Gilles, Palardy, Jean, Patel, Minta, Paul, Terri, Pedersen, Sue, Perron, Patrice, Pesant, Marie-Hélène, Poirier, Paul, Poulin, Marie-Claude, Punthakee, Zubin, Rehman, Waheed, Ross, Stuart, Sagar, P, Saliba, Nouhad, Sandler, Sam, Schiffrin, Alicia, Schlosser, Robert, Seth-Sharma, Anila, Sherman, Mark, Sionit, David, Sivakumar, Tharsan, Soto, Juan, St-Amour, Eric, Steen, Oren, Sussman, Jack, Telner, Adam, Tobe, Sheldon, Twum-Barima, David-Yaw, Van Zanten, Audrey, VanRossum, Nicole, Vecchiarelli, Jonathan, Ward, Rick, Wessengel, John, Weisnagel, Stanley, Wilderman, Igor, Woo, Vincent, Yakubovich, Natalia, Yale, Jean-Francois, Yared, Zeina, Acevedo, Monica, Aguirre, Maria Loreto, Aizman, Andres, Barroso, Maria Soledad, Cobos, Leonardo, Danin Vargas, Alfredo, Descalzi, Barbara, Godoy, Gonzalo, Grumberg, Elio, Lahsen, Rodolfo, Larenas, Gladys, Ortiz, Eugenia, Paredes, Javier, Potthoff, Sergio, Retamal, Eva, Rojas, Luis, Salgado, Manuel, Santibanez, Claudio, Solis, Carmen, Stokins, Benjamin, Accini, Jose, Acebedo, Javier, Agudelo Baena, Lina Maria, Alarcon, Soraya, Angel, Juliana, Arcos, Edgar, Aroca Martinez, M, Atuesta, Leonor, Balaguera, Jose, Ballestas, Doris, Barrera, Sandra Isabel, Barrios Reyes, Rosmy, Bayona, Adolfo, Bermudez, Andres, Bernal, Diego Zarate, Blanquicett, Marco, Bravo, Victor, Bueno, Wendy, Burbano Delgado, Alvaro, Cadena, Alberto, Cadena, Andres, Caicedo, Sandra, Celemin, Carlos, Consuegra, Ricardo, Contreras Pimienta, Cristhian, Corredor, Kelly Johenis, Cure, Carlos, De La Hoz Rueda, Lizeth Dayana, Delgado, Erika, Diaz, Sarahy, Diego, Marta, Donado, Anabell, Encinales Sanabria, William, Escobar, Juliana, Escorcia, Gillian, Forero, Leonardo, Fuentes, Laura, Garcia, Maria, Garcia Lozada, Henry, Garcia Ortiz, Luis, Giraldo, Angela, Gomez Gonzalez, Laura, Granada, Javier, Gutierrez, Corina, Henao, Natalia, Hernandez, Edwin, Herrera Uejbe, Olga Maria, Higuera Cobos, Juan Diego, Ibarra Gómez, Jaime, Jaimes, Edwin Hernandez, Jaramillo, Monica, Jaramillo, Nicolas, Jaramillo Gomez, Carlos, Jaramillo Sanchez, Monica, Jarava Durán, Ivonne, Lopez Ceballos, Catalina, Madrid, Claudia, María Amastha, Elias, Mercado, Jennifer, Molina, Dora Ines, Molina Soto, Jessica, Montoya, Carlos, Morales, Alexander, Muñoz, Carolina, Orozco, Luis Alejandro, Osorio, Oscar, Palmera Sanchez, Jorge Mario, Peña, Adwar, Perez, Jose, Perez Agudelo, Juan, Pérez Amador, Germán, Pertuz, Carlos, Posada, Irina, Puerta, Carlos, Quintero, Adalberto, Quiroz, Diana, Rendon, Carmen, Reyes, Alberto, Reyes, Alvaro, Ripoll, Diana, Rivera, Carlos, Rocha, Maria, Rodriguez, Jose F, Rodriguez Villanueva, Kervis Asid, Rodriguez Zabala, Javier Emilio, Rojas, Sindy, Romero, Maria, Rosero, Ricardo, Rosillo Cardenas, Angelica Rocio, Rueda, Lina, Sanchez, Gregorio, Sanchez, Tatiana, Sotomayor Herazo, Arístides, Suarez, Monica, Torres, Mariana, Trujillo, Freddy, Urina, Miguel, Van Strahlen, Lazaro, Velandia, Carlos, Velasquez Guzman, Carolina, Velazquez, Elizabeth, Vidal Prada, Tatiana, Yepez Alvaran, Juan Pablo, Zarate, Diego, Andelova, Jana, Benesova, Radka, Buzova, Barbara, Cech, Vladimir, Chodova, Ida, Choura, Miroslav, Dufka, Antonin, Gamova, Andrea, Gorgol, Jakub, Hala, Tomas, Havlova, Hana, Hlavkova, Dagmar, Horanska, Petra, Ilcisin-Valova, Juliana, Jenickova, Petra, Jerabek, Ondrej, Kantorova, Ilona, Kolomaznikova, Katerina, Kopeckova, Iva, Kopeckova, Miroslava, Linhart, Karel, Linhart, Tomas, Malecha, Jan, Malicherova, Emilia, Neubauerova, Dana, Oznerova, Martina, Partys, Radan, Pederzoliova, Eva, Petrusova, Maria, Prymkova, Vera, Racicka, Eva, Reissova, Ida, Roderova, Eva, Stanek, Libor, Striova, Alena, Svarcova, Dana, Svoboda, Petr, Szeghy Malicharova, Emilia, Urge, Jan, Vesely, Ladislav, Wasserburger, Bedich, Wasserburgerova, Hilde, Zahumensky, Emil, Zamrazil, Vaclav, Alawi, Hasan, Anastasiadis, Ernestos, Axthelm, Elisabeth, Bieler, Tasso, Buhrig, Christina, Degtyareva, Elizaveta, Dellanna, Frank, Derwahl, Karl-Michael, Diessel, Stephan, Dogiami, Barbara, Dorn-Weitzel, Kirsten, Ernst, Monika, Faulmann, Grit, Fetscher, Baerbel, Forst, Thomas, Freyer-Lahres, Gabriele, Funke, Klaus, Ganz, Xenia, Gleixner, Christiane, Hanefeld, Christoph, Heinrichs, Sven, Helleberg, Stephanie, Henkel, Elena, Hetzel, Gerd Ruediger, Hoffmann, Caren, Jacob, Frohmut, Jacob, Stephan, John, Franziska, Jonczyk, Antonius, Kamke, Wolfram, Klein, Christiane, Kleinhardt, Martina, Kleophas, Werner, Kosch, Christine, Kreutzmann, Kristin, Kühn, Achim, Lee-Barkey, Young Hee, Lier, Alexander, Maatouk, Sarah, Minnich, Joachim, Mitry, Michael, Muessig, Ilona, Nicula, Diana, Niemann, Martina, Nothroff, Joerg, Ott, Petra, Pfuetzner, Andreas, Pfützner, Andreas, Pistrosch, Frank, Pohl, Wildgard, Prochazkova, Zdenka, Retkowska, Marlena, Rosin, Heiko, Sachsenheimer, Daniela, Samer, Holger, Sanuri, Mazin, Schaefer, Axel, Schaper, Frank, Schulze, Erik-Delf, Schulze, Marita, Schumann, Martina, Segiet, Thomas, Sowa, Veronika, Stahl, Hans-Detlev, Steinfeldt, Franziska, Teige, Madlen, Trieb, Bjoern, Tschoepe, Diethelm, Uebel, Peter, Warken, Bernd, Weigmann, Ingo, Weyland, Klaus, Wilhelm, Klara, Balo, Timea, Balsay, Miklos, Bende, Ilona, Bezzegh, Katalin, Birkus, Zita, Buday, Barbara, Csomai, Melinda, Deak, Laszlo, Dezso, Eniko, Faludi, Peter, Faluvegi, M, Fazekas, Ilona, Feher, Agota, Fejer, Csaba, Finta, Ervin, Fulcz, Agnes, Gaal, Zsolt, Gurzo, Mihaly, Hati, Krisztina, Herczeg, Gabriella, Jozsef, Ildiko, Juhasz, Marta, Keltai, Katalin, Koranyi, Laszlo, Kulcsar, Eniko, Kun, Krisztina, Laczko, Andrea, Literáti-Nagy, Botond, Mezo, Izabella, Mileder, Margit, Moricz, I, Nagy, Károly, Nagybaczoni, Bela, Nemeth, Csaba, Oze, Agnes, Pauer, Jozsef, Peterfai, Eva, Polocsanyi, Bela, Poor, Ferenc, Reiber, István, Salamon, Csaba, Sebestyen, Julia, Torok, Ildiko, Tuu, Marianna, Varga, Andrea, Vass, Viktor, Ahn, Chul Min, Ahn, Chulwoo, ByungWon, Park, Chang, Hyuk-Jae, Chang, Kiyuk, Choi, Eui-Young, Choi, Han Seok, Chung, Jin-Wook, Hong, Bum- Kee, Hong, Young Joon, Hyon, Min Su, Jeong, Myung Ho, Kang, Shinae, Kim, Byeong-Keuk, Kim, Ji-Hyun, Kim, Ju Han, Kim, Kee-Sik, Kim, Moo Hyun, Kim, Pum-Joon, Kim, Soon-Kil, Kim, Yong-Seok, Kim, Young Kwon, Koh, Yoon Seok, Kwon, Hyuck Moon, Lee, Byoung Kwon, Lee, Byung-Wan, Lee, Jin Bae, Lee, Myoung-Mook, Lim, Young-Mee, Min, Pil Ki, Park, Jong Sung, Park, Jongsuk, Park, Keun Ho, Park, Sungha, Pyun, Wook Bum, Rim, Se Joong, Ryu, Dong-Ryeol, Seo, Hong-Seog, Seung, Ki Bae, Shin, Dong-Ho, Sim, Doo Sun, Yoon, Young Won, Andersone, Ilze, Babicka, Kristine, Balcere, Inga, Barons, Roberts, Capkovska, Inguna, Geldnere, Kristine, Grigane, Inese, Jegere, Baiba, Lagzdina, Ilze, Mora, Lija, Pastare, Sigita, Ritenberga, Rota, Romanova, Janina, Saknite, Inta, Sidlovska, Natalja, Sokolova, Jelena, Steina, Sandra, Strizko, Iveta, Teterovska, Dace, Vizina, Brigita, Barsiene, Lina, Belozariene, Gintare, Daugintyte-Petrusiene, Laura, Drungiliene, Nijole, Garsviene, Nijole, Grigiene, Ala, Grizas, Vytautas, Jociene, Virginija, Kalvaitiene, Dalia, Kaupiene, Jugeta, Kavaliauskiene, Jurate, Kozloviene, Dalia, Lapteva, Ilona, Maneikiene, Birute, Marcinkeviciene, Jolanta, Markauskiene, Vaidilija, Meiluniene, Salomeja, Norkus, Almantas, Norviliene, Rita, Petrenko, Vladimiras, Radzeviciene, Ruta, Sakalyte, Gintare, Urbonas, Gediminas, Urbutiene, Skaiste, Vasiliauskas, Donatas, Velickiene, Dzilda, Aguilar, Carlos, Alcocer, Marco, Avalos-Ramirez, Juan Antonio, Banda-Elizondo, Ramiro, Bricio-Ramirez, Rubria, Cardenas Mejia, Karla, Cavazos, Francisco, Chapa, Jesus, Cienfuegos, Erika, De la Peña, Astrid, de la Peña Topete, Gilberto, De los Rios Ibarra, Manuel Odin, Elias, Daniel, Flores-Moreno, Claudia, Garcia Hernandez, Pedro, Gonzalez, Luis Gerardo, Guerra Moya, Rosa Linda, Guerra-Lopez, Arturo, Hernandez Baylon, Raymundo, Herrera Colorado, Carolina, Herrera-Marmolejo, Marisol, Islas-Palacios, Neri, Lopez, Esteban, Lopez, Fernando, Lopez Alvarado, Agustin, Luna Ceballos, Rosa Isela, Morales Villegas, Enrique, Moreno-Virgen, Gualberto, Parra Perez, Rosa Linda, Pascoe Gonzalez, Sara, Peralta-Cantu, Irving, Previn, Roopa, Ramirez, Rosa, Ramirez, Rubria, Ramos Zavala, Maria Guadalupe, Rodriguez, Monica, Salgado-Sedano, Rocio, Sanchez-Aguilar, Ana Claudia, Santa Rosa Franco, Edith, Sauque-Reyna, Leobardo, Suarez Otero, Rodrigo, Torres, Ivonne, Velarde-Harnandez, Enrique, Villagordoa, Juan, Villeda-Espinoza, Efrain, Vital-Lopez, Jorge, Zavala- Bello, Cristian Jair, Baker, John, Barrington-Ward, Elaine, Brownless, Thomas, Carroll, Richard, Carson, Simon, Choe, Michelle, Corin, Andrew, Corley, Brian, Cutfield, Richard, Dalaman, Neelam, Dixon, Paul, Drury, Paul, Dyson, Keith, Florkowski, Chris, Ford, Monica, Frengley, William, Helm, Colin, Katzen, Colin, Kerr, Jane, Khanolkar, Manish, Kim, David, Koops, Renata, Krebs, Jeremy, Leikis, Robert, Low, Kwan, Luckey, Alison, Luke, Richard, Macaulay, Susan, Marks, Rodney, McNamara, Catherine, Millar-Coote, Dean, Miller, Steven, Mottershead, Naomi, Reid, James, Robertson, Narcisa, Rosen, Ian, Rowe, David, Schmiedel, Ole, Scott, Russell, Sebastian, Jeffrey, Sheahan, Davitt, Stiebel, Victoria, Ternouth, Ian, Tofield, Chris, Venter, Dirk, Williams, Michael, Williams, Miles, Wu, Fiona, Young, Simon, Arciszewska, Malgorzata, Bochenek, Anna, Borkowski, Piotr, Borowy, Przemyslaw, Chrzanowski, Tomasz, Czerwinski, Edward, Dwojak, Marek, Grodzicka, Agnieszka, Janiec, Izabela, Jaruga, Joanna, Jazwinska-Tarnawska, Ewa Krystyna, Jedynasty, Krystyna, Juzwiak-Czapiewska, Danuta, Karczewicz-Janowska, Jadwiga, Konieczny, Jan, Konieczny, Marek, Korol, Marek, Kozina, Maciej, Krzyzagorska, Ewa, Kucharczyk-Petryka, Ewa, Laz, Roman, Majchrzak, Anna, Mrozowska, Zdzislawa, Mularczyk, Michal, Nowacka, Elzbieta, Peczynska, Jadwiga, Petryka, Robert, Pietrzak, Radoslaw, Pisarczyk-Wiza, Dorota, Rozanska, Aleksandra, Ruzga, Zofia, Rzeszotarska, Emilia, Sacha, Malgorzata, Sekulska, Marzenna, Sidorowicz-Bialynicka, Anna, Stasinska, Teresa, Strzelecka-Sosik, Agnieszka, Swierszcz, Teresa, Szymkowiak, Katarzyna Miroslawa, Turowska, Olga, Wisniewska, Krystyna, Wiza, Maciej, Wozniak, Iwona, Zelazowska, Katarzyna, Ziolkowska-Gawron, Bernadetta, Zytkiewicz-Jaruga, Danuta, Albota, Adrian, Alexandru, Carmina, Avram, Rodica, Bala, Cornelia, Barbonta, Diana, Barbu, Roxana, Braicu, Daniela, Calutiu, Nicoleta, Catrinoiu, Doina, Cerghizan, Anca, Ciorba, Alina, Craciun, Anca, Doros, Rodica, Duma, Livia, Dumitrache, Ancuta, Ferariu, Ioana, Ferician Moza, Anca, Ghergan, Alexandrina, Ghise, Gheorghe, Graur, Mariana, Gribovschi, Mihaela, Mihai, Bogdan, Mihalache, Laura, Mihalcea, Madalina, Mindrescu, Nicoleta, Morosanu, Magdalena, Morosoanu, Andrea, Mota, Maria, Moza, Anca, Nafornita, Valerica, Natea, Narcisa, Nicodim, Simona, Nita, Cristina, Onaca, Adriana, Onaca, Mircea, Pop, Cristina, Pop, Lavinia, Popa, Amorin, Popescu, Alexandrina, Pruna, Luchiana, Roman, Gabriela, Rosu, Mihaela, Sima, Alexandra, Sipciu, Doina, Sitterli-Natea, Carmen Narcisa, Szilagyi, Iosif, Tapurica, Minodora, Tase, Adrian, Tutescu, Adriana-Carmen, Vanghelie, Luminita, Verde, Ioana, Vlad, Adrian, Zarnescu, Mihaela, Akhmetov, Roman, Allenova, Irina, Avdeeva, Irina, Baturina, Oksana, Biserova, Irina, Bokovin, Nikolay, Bondar, Irina, Burova, Natalia, Chufeneva, Galina, Chumachek, Elena, Demidova, Marina, Demin, Alexander, Drobysheva, Vera, Egorova, Irina, Esenyan, Lev, Gelig, Ekaterina, Gilyarevsky, Sergey, Golshmid, Maria, Goncharov, Arseniy, Gorbunova, Anastasia, Gordeev, Ivan, Gorelysheva, Vera, Goryunova, Tatiana, Grebenshchikova, Irina, Ilchenko, Roman, Ivannikova, Maria, Karabalieva, Saule, Karpeeva, Juliya, Khaykina, Elena, Kobalava, Zhanna, Kononenko, Irina, Korolik, Oxana, Korshunova, Anna, Kostenko, Victor, Krasnopevtseva, Irina, Krylova, Ludmila, Kulkova, Polina, Kuzmina, Irina, Ledyaeva, Alla, Levashov, Sergey, Lokhovinina, Natalia, Lvov, Vadim, Martirosyan, Narine, Nedogoda, Sergey, Nilk, Rostislav, Osmolovskaya, Yulia, Panov, Alexey, Paramonova, Olga, Pavlova, Ekaterina, Pekareva, Elena, Petunina, Nina, Ponamareva, Svetlana, Reshedko, Galina, Salasyuk, Alla, Sepkhanyan, Malvina, Serebrov, Alexandr, Shabelnikova, Olesya, Skvortsov, Andrey, Smirnova, Olga, Spiridonova, Oxana, Strogova, Svetlana, Taratukhin, Evgeny, Tereschenko, Sergey, Trukhina, Lubov, Tsarkova, Olga, Tsoma, Vera, Tumarov, Farid, Tyan, Natalya, Tyurina, Tatiana, Villevalde, Svetlana, Yankovaya, Elena, Zarutskaya, Ludmila, Zenkova, Elena, Badat, Aysha, Bester, Frederik, Blignaut, Suzanne, Blom, Dirk, Booysen, Susan, Boyd, Warren, Brice, Brigitte, Brown, Susan, Burgess, Lesley, Cawood, Reina, Coetzee, Kathleen, Conradie, Hillet, Cronje, Tanja, de Jong, Douwe, Ellis, Graham, Emanuel, Shaunagh, Engelbrecht, Ingrid, Foulkes, Sharne, Fourie, Done, Gibson, Gilbert, Govender, Thirumani, Hansa, Sumayah, Hemus, Allana Colleen, Hendricks, Firzana, Heradien, Marshall, Holmgren, Chantelle, Hoosain, Zaheer, Horak, Emile, Howard, Johannes, Immink, Ignatius, Janari, E., Jivan, Daksha, Klusmann, Karl, Labuschagne, Weik, Lai, Yen-yu, Latiff, Gulam, Lombaard, J., Lottering, Hanlie, Meeding, Ronel, Middlemost, Shirley, Mitha, Haroon, Mitha, Ismail, Mkhwanazi, Sandile, Moodley, Rajendran, Murray, Almeri, Musungaie, Dany, Osman, Yasmin, Peacey, Kirsten, Pillay-Ramaya, Larisha, Pretorius, Catharina, Prozesky, Hans, Sarvan, Mahomed, Scholtz, E, Sebesteny, Attila, Skinner, Bianca, Skriker, Michael, Smit, M, Stapelberg, Anna-Marie, Swanepoel, Nicolaas, Urbach, Dorothea, van Aswegen, Dina, van Zyl, Francois, Van Zyl, Louis, Venter, Esme, Wadvalla, Shahid, Wing, Jeffrey, Wolmarans, Karen, Abreu, Cristina, Aguilà, Pilar, Aguilera, Eva, Alonso, Nuria, Alvarez, Carmen, Cajas, Priscila, Castro, Jose Carlos, Codinachs, Roger, Contreras, Jose, Coves, Maria Jose, Fajardo, Carmen, Ferrer, Juan Carlos, Font, Neus, Garcia, Mar, Gil, Maria Apolonia, Gomez, Fernando, Gomez, Lluis Alberto, Gonzalbez, Jose, Griera, Jose Luis, Masmiquel, Luís, Mauricio, Didac, Narejos Perez, Silvia, Nicolau, Juana Ana, Noheda Contreras, Olga, Olivan, Josefina, Olivares, Josefina, Ortega, Emilio, Pellitero, Silvia, Pertusa, Salvador, Rius, Ferran, Rodriguez, Irene, Sánchez-Juan, Carlos, Santos, Dolores, Soldevila, Berta, Subias, David, Terns, Manel, Trescoli, Carlos, Vilaplana, Judith, Villanueva, Alicia, Albo, Jaan, Antus, Kjell, Axelsson, Mattias, Bergström, Lisa, Binsell-Gerdin, Emil, Boman, Kurt, Botond, Fabian, Dotevall, Annika, Graipe, Anna, Jarnet, C, Kaminska, Jessica, Kempe, Anders, Korhonen, Michael, Linderfalk, Carina, Liu, Bo, Ljungstroem, Karl, Ljungström, Karl, Malmqvist, Lennart, Mellbin, Linda, Mooe, Thomas, Nicol, Peter, Norrby, Anders, Ohlsson, Ake, Rosengren, Annika, Saaf, Jan, Salmonsson, Staffan, Strandberg, Olof, Svensson, Karl-Axel, Tengmark, Bengt-Olov, Tsatsaris, Georgios, Ulvenstam, Anders, Vasko, Peter, Chang, Chwen-Tzuei, Chang, Hsin-Mei, Chen, Jung-Fu, Chen, To-Pang, Chung, Ming-Min, Fu, Chia-Po, Hsia, Te-Lin, Hua, Shih-Che, Kuo, Ming-Chun, Lee, Chia-ln, Lee, I-Te, Liang, Kae-Woei, Lin, Shih Yi, Lu, Chieh-Hsiang, Ma, Wen-Ya, Pei, Dee, Shen, Feng-Chih, Su, Ching-Chieh, Su, Shuo-Wei, Tai, Tsai-Sung, Tsai, Wan-Ni, Tsai, Yi-Ting, Tung, Shih-Chen, Wang, Jun-Sing, Yu, Hui-I, Al-Qaissi, Ahmed, Arutchelvam, Vijayaraman, Atkin, Stephen, Au, Simon, Aye, Myint Myint, Bain, Stephen, Bejnariu, Cristina, Bell, Patrick, Bhatnagar, Deepak, Bilous, Rudy, Black, Neil, Brennan, Ursula, Brett, Barbara, Bujanova, Jana, Chow, Elaine, Collier, Andrew, Combe, Amanda, Courtney, Christopher, Courtney, Hamish, Crothers, James, Eavis, Patrick, Elliott, Jackie, Febbraro, Salvatore, Finlayson, Jim, Gandhi, Rajiv, Gillings, Sharon, Hamling, Jonathan, Harper, Roy, Harris, Tim, Hassan, Kahal, Heller, Simon, Jane, Alison, Javed, Zeeshan, Johnson, Tim, Jones, Stephen, Kennedy, Adele, Kerr, David, Kilgallon, Brian, Konya, Judith, Lindsay, John, Lomova-Williams, Lina, Looker, Helen, MacFarlane, David, Macrury, Sandra, Malik, Iqbal, McCrimmon, Rory, McKeith, Douglas, McKnight, John, Mishra, Biswa, Mukhtar, Racha, Mulligan, Ciara, O'Kane, Maurice, Olateju, Tolu, Orpen, Ian, Richardson, Tristan, Rooney, Desmond, Ross, Shorsha Bae, Sathyapalan, Thozhukat, Siddaramaiah, Naveen, Sit, Lee Euan, Stephens, Jeffrey, Turtle, Frances, Wakil, Ammar, Walkinshaw, Emma, Ali, Asem, Anderson, Robert, Arakaki, Richard, Aref, Omar, Ariani, Mehrdad Kevin, Arkin, David, Banarer, Salomon, Barchini, George, Bhan, Arti, Branch, Kelley, Brautigam, Donald, Brietzke, Stephen, Brinas, Maridez, Brito, Yudit, Carter, Casey, Casagni, Kimberely, Casula, Sabina, Chakko, Simon, Charatz, Seth, Childress, Dale, Chow, Lisa, Chustecka, Malgorzata, Clarke, Subha, Cohen, Lisa, Collins, Barry, Colon Vega, Gildred, Comulada-Rivera, Angel, Cortes-Maisonet, Gregorio, Davis, Matthew, de Souza, Jose, Desouza, Cyrus, Dinnan, Mary, Duffy-Hidalgo, Bobbi, Dunn, Barbara, Dunn, Julia, Elman, Marshall, Felicetta, James, Finkelstein, Stuart, Fitz-Patrick, David, Florez, Hermes, Forker, Alan, Fowler, Wayne, Fredrickson, Sonja, Freedman, Zachary, Gainey Narron, Brooke, Gainey-Ferree, Kristin, Gardner, Michael, Gastelum, Christian, Giddings, Stephen, Gillespie, Eve, Gimness, Michael Paul, Goldstein, Gary, Gomes, Maria, Gomez, Nelson, Gorman, Timothy, Goswami, Ketan, Graves, Arthur, Hacking, Scott, Hall, Charles, Hanson, Lenita, Harman, Sherman, Heber, David, Henry, Robert, Hiner, Janette, Hirsch, Irl, Hollander, Priscilla, Hooker, Thomas, Horowitz, Barry, Hoste, Laura, Huang, Loli, Huynh, Minh, Hyman, Dan, Idriss, Soha, Iranmanesh, Ali, Karounos, Dennis, Kashyap, Moti, Katz, Lois, Kaye, William, Khaiton, Yevgeniy, Khardori, Romesh, Kitchen, Timothy, Klein, Andrew, Knffem, Wendi, Kosiborod, Mikhail, Kreglinger, Nicola, Kruger, Davida, Kumar, Anubhav, Laboy, Ivan, Larrabee, Patricia, Larrick, Laura, Lawson, Donna, Ledet, Mike, Lenhard, James, Levy, James, Li, George, Li, Zhaoping, Lieb, David, Limcolioc, April, Lions-Patterson, Jane, Lorber, Daniel, Lorch, Daniel, Lorrello, Michael, Lu, Peter, Lucas, Kathryn Jean, Ma, Siu-Ling, MacAdams, Michael, Magee, Michelle, Magno, Alexander, Mahakala, Aparna Reddy, Marks, Jennifer, McCall, Anthony, McClanahan, William, Jr., McClary, Carole, Melendez, Lydia, Melish, John, Michaud, Deanna, Miller, Christopher, Miller, Neil, Mora, Pablo, Moten, Marriyam, Mudaliar, Sunder, Myrick, Gregory, Narayan, Puneet, Nassif, Mike, Neri, Karena, Newton, Tabitha, Niblack, Patricia, Nicol, Philip, Nyenwe, Ebenezer, Odugbesan, A. Ola, Okorocha, Yolanda, Ortiz Carrasquillo, Ramón, Osei, Kwame, Palermo, Coromoto, Patel, Hiren, Patel, Krishna, Pau, Cindy, Perley, Michael, Plevin, Sanford, Plummer, Elena, Powell, Richard, Qintar, Mohammed, Rawls, Rex, Reyes-Castano, John, Reynolds, Lillian, Richards, Robert, Rosenstock, Julio, Rowe, Caroline, Saleh, Jahandar, Sam, Sony, Sanchez, Alfredo, Sander, Donald, Sanderson, Bruce, Savin, Virginia, Seaquist, Elizabeth, Shah, Jayendra, Shi, Serena, Shivaswamy, Vijay, Shlotzhauer, Tammi, Shore, David, Skukowski, Bobbie, Soe, Kyaw, Solheim, Vesna, Soufer, Joseph, Steinberg, Helmut, Steinsapir, Jaime, Tarkington, Phillip, Thayer, Debra, Thomson, Stephen, Thrasher, James, Tibaldi, Joseph, Tjaden, Jeff, Tores, Oberto, Trence, Dace, Trikudanathan, Subbulaxmi, Ullal, Jagdeesh, Uwaifo, Gabriel, Vo, Anthony, Vu, Kenny, Walia, Damandeep, Weiland, Karen, Whitehouse, Fred, Wiegmann, Thomas, Wyne, Kathleen, Wynne, Alan, Yuen, Kevin, Zaretzky, Joel, Zebrack, James, Zieve, Franklin, Zigrang, William, Gerstein, Hertzel C, Colhoun, Helen M, Dagenais, Gilles R, Diaz, Rafael, Lakshmanan, Mark, Pais, Prem, Probstfield, Jeffrey, Riesmeyer, Jeffrey S, Riddle, Matthew C, Rydén, Lars, Xavier, Denis, Atisso, Charles Messan, Dyal, Leanne, Hall, Stephanie, Rao-Melacini, Purnima, Wong, Gloria, Avezum, Alvaro, Basile, Jan, Chung, Namsik, Conget, Ignacio, Cushman, William C, Franek, Edward, Hancu, Nicolae, Hanefeld, Markolf, Holt, Shaun, Jansky, Petr, Keltai, Matyas, Lanas, Fernando, Leiter, Lawrence A, Lopez-Jaramillo, Patricio, Cardona Munoz, Ernesto German, Pirags, Valdis, Pogosova, Nana, Raubenheimer, Peter J, Shaw, Jonathan E, Sheu, Wayne H-H, and Temelkova-Kurktschiev, Theodora
Published: 2019
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38. High-resolution Inference of Multiplexed Anti-HIV Gene Editing using Single-Cell Targeted DNA Sequencing

Author: Bouzidi, Mohamed, primary, Dossani, Zain, additional, Di Benedetto, Carolina, additional, Raymond, Kyle, additional, Desai, Shivani, additional, Chavez, Leonard, additional, Betancur, Paola, additional, and Pillai, Satish K., additional
Published: 2024
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39. Decreased HIV Type 1 Transcription in CCR5-Δ32 Heterozygotes During Suppressive Antiretroviral Therapy

Author: Wang, Charlene, Abdel-Mohsen, Mohamed, Strain, Matthew C, Lada, Steven M, Yukl, Steven, Cockerham, Leslie R, Pilcher, Christopher D, Hecht, Frederick M, Sinclair, Elizabeth, Liegler, Teri, Richman, Douglas D, Deeks, Steven G, and Pillai, Satish K
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Sexually Transmitted Infections, HIV/AIDS, Genetics, 5.1 Pharmaceuticals, Infection, Antiretroviral Therapy, Highly Active, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cohort Studies, Gene Expression Regulation, Viral, Genotype, HIV Infections, HIV-1, Heterozygote, Humans, Mutation, Phenotype, RNA, Viral, Receptors, CCR5, Viral Load, HIV, CCR5, Delta 32, coreceptor, reservoir, latency, eradication, NF-kappa B, HIV transcription, HIV replication, NF-κB, Δ32, Biological Sciences, Medical and Health Sciences, Microbiology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract: Individuals who are heterozygous for the CCR5-Δ32 mutation provide a natural model to examine the effects of reduced CCR5 expression on human immunodeficiency virus (HIV) persistence. We evaluated the HIV reservoir in 18 CCR5-Δ32 heterozygotes and 54 CCR5 wild-type individuals during suppressive antiretroviral therapy. Cell-associated HIV RNA levels (P=.035), RNA to DNA transcriptional ratios (P=.013), and frequency of detectable HIV 2-long terminal repeat circular DNA (P=.013) were significantly lower in CD4+ T cells from CCR5-Δ32 heterozygotes. Cell-associated HIV RNA was significantly correlated with CCR5 surface expression on CD4+ T cells (r2=0.136; P=.002). Our findings suggest that curative strategies should further explore manipulation of CCR5.
Published: 2014

40. Dynamic Regulation of Host Restriction Factor Expression over the Course of HIV-1 Infection In Vivo

Author: Raposo, Rui André Saraiva, Abdel-Mohsen, Mohamed, Deng, Xutao, Hecht, Frederick M, Pilcher, Christopher D, Pillai, Satish K, and Nixon, Douglas F
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, HIV/AIDS, Infectious Diseases, 2.2 Factors relating to the physical environment, Infection, Adult, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes, Gene Expression Profiling, Gene Expression Regulation, HIV Infections, HIV-1, Host-Pathogen Interactions, Humans, Longitudinal Studies, Lymphocyte Activation, Male, RNA, Viral, Repressor Proteins, Viral Load, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract: In this study, we investigated the expression levels of host restriction factors in six untreated HIV-1-positive patients over the course of infection. We found that the host restriction factor gene expression profile consistently increased over time and was significantly associated with CD4+ T cell activation and viral load. Our data are among the first to demonstrate the dynamic nature of host restriction factors in vivo over time.
Published: 2014

41. Pharmacy Needs After a Natural Disaster — Puerto Rico, September–October 2017

Author: Lavery, Amy M., Patel, Anita, Boehmer, Tegan K., Lee, Leslie, Bhavsar, Tina, Thomas, Jacqueline, Hall, Lori, Beavers, Suzanne, Murray, Maria, and Pillai, Satish K.
Published: 2018

42. Initial Public Health Laboratory Response After Hurricane Maria — Puerto Rico, 2017

Author: Concepción-Acevedo, Jeniffer, Patel, Anita, Luna-Pinto, Carolina, Peña, Rafael González, Ruiz, Rosa Ivette Cuevas, Arbolay, Héctor Rivera, Toro, Mayra, Deseda, Carmen, De Jesus, Victor R., Ribot, Efrain, Gonzalez, Jennifer-Quiñones, Rao, Gouthami, De Leon Salazar, Alfonsina, Ansbro, Marisela, White, Brunilís B., Hardy, Margaret C., Georgi, Joaudimir Castro, Stinnett, Rita, Mercante, Alexandra M., Lowe, David, Martin, Haley, Starks, Angela, Metchock, Beverly, Johnston, Stephanie, Dalton, Tracy, Joglar, Olga, Stafford, Cortney, Youngblood, Monica, Klein, Katherine, Lindstrom, Stephen, Berman, LaShondra, Galloway, Renee, Schafer, Ilana J., Walke, Henry, Stoddard, Robyn, Connelly, Robin, McCaffery, Elaine, Rowlinson, Marie-Claire, Soroka, Stephen, Tranquillo, Darin T., Gaynor, Anne, Mangal, Chris, Wroblewski, Kelly, Muehlenbachs, Atis, Salerno, Reynolds M., Lozier, Matthew, Sunshine, Brittany, Shapiro, Craig, Rose, Dale, Funk, Renee, Pillai, Satish K., and O’Neill, Eduardo
Published: 2018

43. Effects of Alpha Interferon Treatment on Intrinsic Anti-HIV-1 Immunity In Vivo

Author: Abdel-Mohsen, Mohamed, Deng, Xutao, Liegler, Teri, Guatelli, John C, Salama, Mohamed S, Ghanem, Hussam El-din A, Rauch, Andri, Ledergerber, Bruno, Deeks, Steven G, Günthard, Huldrych F, Wong, Joseph K, and Pillai, Satish K
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Hepatitis, Hepatitis - C, Emerging Infectious Diseases, HIV/AIDS, Liver Disease, Sexually Transmitted Infections, Infectious Diseases, Digestive Diseases, 5.1 Pharmaceuticals, Infection, Good Health and Well Being, HIV, Interferon-alpha, Ribavirin, Virus Replication, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract: Alpha interferon (IFN-α) suppresses human immunodeficiency virus type 1 (HIV-1) replication in vitro by inducing cell-intrinsic retroviral restriction mechanisms. We investigated the effects of IFN-α/ribavirin (IFN-α/riba) treatment on 34 anti-HIV-1 restriction factors in vivo. Expression of several anti-HIV-1 restriction factors was significantly induced by IFN-α/riba in HIV/hepatitis C virus (HCV)-coinfected individuals. Fold induction of cumulative restriction factor expression in CD4(+) T cells was significantly correlated with viral load reduction during IFN-α/riba treatment (r(2) = 0.649; P < 0.016). Exogenous IFN-α induces supraphysiologic restriction factor expression associated with a pronounced decrease in HIV-1 viremia.
Published: 2014

44. Expression profile of host restriction factors in HIV-1 elite controllers

Author: Abdel-Mohsen, Mohamed, Raposo, Rui André, Deng, Xutao, Li, Manqing, Liegler, Teri, Sinclair, Elizabeth, Salama, Mohamed S, Ghanem, Hussam, Hoh, Rebecca, Wong, Joseph K, David, Michael, Nixon, Douglas F, Deeks, Steven G, and Pillai, Satish K
Abstract: Abstract Background Several host-encoded antiviral factors suppress HIV-1 replication in a cell-autonomous fashion in vitro. The relevance of these defenses to the control of HIV-1 in vivo remains to be elucidated. We hypothesized that cellular restriction of HIV-1 replication plays a significant role in the observed suppression of HIV-1 in "elite controllers", individuals who maintain undetectable levels of viremia in the absence of antiretroviral therapy (ART). We comprehensively compared the expression levels of 34 host restriction factors and cellular activation levels in CD4+ T cells and sorted T cell subsets between elite controllers, HIV-1-infected (untreated) non-controllers, ART-suppressed, and uninfected individuals. Results Expression of schlafen 11, a codon usage-based inhibitor of HIV-1 protein synthesis, was significantly elevated in CD4+ T cells from elite controllers as compared to both non-controllers (p = 0.048) and ART-suppressed individuals (p = 0.024), with this effect most apparent in central memory CD4+ T cells. Schlafen 11 expression levels were comparable between controllers and uninfected individuals. Cumulative restriction factor expression was positively correlated with CD4+ T cell activation (r2 = 0.597, p
Published: 2013

45. Challenges in Detecting HIV Persistence during Potentially Curative Interventions: A Study of the Berlin Patient

Author: Yukl, Steven A, Boritz, Eli, Busch, Michael, Bentsen, Christopher, Chun, Tae-Wook, Douek, Daniel, Eisele, Evelyn, Haase, Ashley, Ho, Ya-Chi, Hütter, Gero, Justement, J Shawn, Keating, Sheila, Lee, Tzong-Hae, Li, Peilin, Murray, Danielle, Palmer, Sarah, Pilcher, Christopher, Pillai, Satish, Price, Richard W, Rothenberger, Meghan, Schacker, Timothy, Siliciano, Janet, Siliciano, Robert, Sinclair, Elizabeth, Strain, Matt, Wong, Joseph, Richman, Douglas, and Deeks, Steven G
Subjects: Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Biotechnology, Clinical Research, Transplantation, HIV/AIDS, Sexually Transmitted Infections, Infectious Diseases, Genetics, 4.1 Discovery and preclinical testing of markers and technologies, Infection, Adult, Allografts, Anti-Retroviral Agents, Antibodies, Viral, DNA, Viral, HIV, HIV Infections, Hematopoietic Stem Cell Transplantation, Humans, RNA, Viral, Microbiology, Virology, Medical microbiology
Abstract: There is intense interest in developing curative interventions for HIV. How such a cure will be quantified and defined is not known. We applied a series of measurements of HIV persistence to the study of an HIV-infected adult who has exhibited evidence of cure after allogeneic hematopoietic stem cell transplant from a homozygous CCR5Δ32 donor. Samples from blood, spinal fluid, lymph node, and gut were analyzed in multiple laboratories using different approaches. No HIV DNA or RNA was detected in peripheral blood mononuclear cells (PBMC), spinal fluid, lymph node, or terminal ileum, and no replication-competent virus could be cultured from PBMCs. However, HIV RNA was detected in plasma (2 laboratories) and HIV DNA was detected in the rectum (1 laboratory) at levels considerably lower than those expected in ART-suppressed patients. It was not possible to obtain sequence data from plasma or gut, while an X4 sequence from PBMC did not match the pre-transplant sequence. HIV antibody levels were readily detectable but declined over time; T cell responses were largely absent. The occasional, low-level PCR signals raise the possibility that some HIV nucleic acid might persist, although they could also be false positives. Since HIV levels in well-treated individuals are near the limits of detection of current assays, more sensitive assays need to be developed and validated. The absence of recrudescent HIV replication and waning HIV-specific immune responses five years after withdrawal of treatment provide proof of a clinical cure.
Published: 2013

46. Human Endogenous Retrovirus K106 (HERV-K106) Was Infectious after the Emergence of Anatomically Modern Humans

Author: Jha, Aashish R, Nixon, Douglas F, Rosenberg, Michael G, Martin, Jeffrey N, Deeks, Steven G, Hudson, Richard R, Garrison, Keith E, and Pillai, Satish K
Subjects: Biological Sciences, Genetics, Infectious Diseases, Good Health and Well Being, Base Sequence, Binding Sites, Endogenous Retroviruses, Evolution, Molecular, Genome, Human, Genome, Viral, Humans, Molecular Sequence Data, Mutagenesis, Insertional, Phylogeny, Proviruses, Terminal Repeat Sequences, Time Factors, General Science & Technology
Abstract: HERV-K113 and HERV-K115 have been considered to be among the youngest HERVs because they are the only known full-length proviruses that are insertionally polymorphic and maintain the open reading frames of their coding genes. However, recent data suggest that HERV-K113 is at least 800,000 years old, and HERV-K115 even older. A systematic study of HERV-K HML2 members to identify HERVs that may have infected the human genome in the more recent evolutionary past is lacking. Therefore, we sought to determine how recently HERVs were exogenous and infectious by examining sequence variation in the long terminal repeat (LTR) regions of all full-length HERV-K loci. We used the traditional method of inter-LTR comparison to analyze all full length HERV-Ks and determined that two insertions, HERV-K106 and HERV-K116 have no differences between their 5' and 3' LTR sequences, suggesting that these insertions were endogenized in the recent evolutionary past. Among these insertions with no sequence differences between their LTR regions, HERV-K106 had the most intact viral sequence structure. Coalescent analysis of HERV-K106 3' LTR sequences representing 51 ethnically diverse individuals suggests that HERV-K106 integrated into the human germ line approximately 150,000 years ago, after the emergence of anatomically modern humans.
Published: 2011

47. The Epidemiology of Foodborne Botulism Outbreaks : A Systematic Review

Author: Fleck-Derderian, Shannon, Shankar, Manjunath, Rao, Agam K., Chatham-Stephens, Kevin, Adjei, Stacey, Sobel, Jeremy, Meltzer, Martin I., Meaney-Delman, Dana, and Pillai, Satish K.
Published: 2018

48. In vivo CD8+ T-cell suppression of siv viremia is not mediated by CTL clearance of productively infected cells.

Author: Wong, Joseph K, Strain, Matthew C, Porrata, Rodin, Reay, Elizabeth, Sankaran-Walters, Sumathi, Ignacio, Caroline C, Russell, Theresa, Pillai, Satish K, Looney, David J, and Dandekar, Satya
Subjects: CD8-Positive T-Lymphocytes, T-Lymphocytes, Cytotoxic, Animals, Macaca mulatta, Viremia, Simian Acquired Immunodeficiency Syndrome, Gene Products, nef, Gene Products, gag, Anti-Retroviral Agents, Viral Load, Gene Expression, Models, Theoretical, Simian immunodeficiency virus, Simian Immunodeficiency Virus, T-Lymphocytes, Cytotoxic, Gene Products, nef, gag, Models, Theoretical, Virology, Microbiology, Immunology, Medical Microbiology
Abstract: The CD8+ T-cell is a key mediator of antiviral immunity, potentially contributing to control of pathogenic lentiviral infection through both innate and adaptive mechanisms. We studied viral dynamics during antiretroviral treatment of simian immunodeficiency virus (SIV) infected rhesus macaques following CD8+ T-cell depletion to test the importance of adaptive cytotoxic effects in clearance of cells productively infected with SIV. As previously described, plasma viral load (VL) increased following CD8+ T-cell depletion and was proportional to the magnitude of CD8+ T-cell depletion in the GALT, confirming a direct relationship between CD8+ T-cell loss and viral replication. Surprisingly, first phase plasma virus decay following administration of antiretroviral drugs was not slower in CD8+ T-cell depleted animals compared with controls indicating that the short lifespan of the average productively infected cell is not a reflection of cytotoxic T-lymphocyte (CTL) killing. Our findings support a dominant role for non-cytotoxic effects of CD8+ T-cells on control of pathogenic lentiviral infection and suggest that cytotoxic effects, if present, are limited to early, pre-productive stages of the viral life cycle. These observations have important implications for future strategies to augment immune control of HIV.
Published: 2010

49. Systematic benchmarking of single-cell ATAC-sequencing protocols

Author: De Rop, Florian V., primary, Hulselmans, Gert, additional, Flerin, Chris, additional, Soler-Vila, Paula, additional, Rafels, Albert, additional, Christiaens, Valerie, additional, González-Blas, Carmen Bravo, additional, Marchese, Domenica, additional, Caratù, Ginevra, additional, Poovathingal, Suresh, additional, Rozenblatt-Rosen, Orit, additional, Slyper, Michael, additional, Luo, Wendy, additional, Muus, Christoph, additional, Duarte, Fabiana, additional, Shrestha, Rojesh, additional, Bagdatli, S. Tansu, additional, Corces, M. Ryan, additional, Mamanova, Lira, additional, Knights, Andrew, additional, Meyer, Kerstin B., additional, Mulqueen, Ryan, additional, Taherinasab, Akram, additional, Maschmeyer, Patrick, additional, Pezoldt, Jörn, additional, Lambert, Camille Lucie Germaine, additional, Iglesias, Marta, additional, Najle, Sebastián R., additional, Dossani, Zain Y., additional, Martelotto, Luciano G., additional, Burkett, Zach, additional, Lebofsky, Ronald, additional, Martin-Subero, José Ignacio, additional, Pillai, Satish, additional, Sebé-Pedrós, Arnau, additional, Deplancke, Bart, additional, Teichmann, Sarah A., additional, Ludwig, Leif S., additional, Braun, Theodore P., additional, Adey, Andrew C., additional, Greenleaf, William J., additional, Buenrostro, Jason D., additional, Regev, Aviv, additional, Aerts, Stein, additional, and Heyn, Holger, additional
Published: 2023
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50. A Novel Viral Assembly Inhibitor Blocks SARS-CoV-2 Replication in Airway Epithelial Cells

Author: Pillai, Satish, primary, Du, Li, additional, Deiter, Fred, additional, Bouzidi, Mohamed, additional, Billaud, Jean-Noel, additional, Graham, Simmons, additional, Prerna, Dabral, additional, Selvarajah, Suganya, additional, Lingappa, Anuradha, additional, Michon, Maya, additional, Yu, Shao, additional, Paulvannan, Kumar, additional, Lingappa, Vishwanath, additional, Boushey, Homer, additional, and Greenland, John, additional
Published: 2023
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