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2. Malaria-driven adaptation of MHC class I in wild bonobo populations

Author

Wroblewski, Emily E., Guethlein, Lisbeth A., Anderson, Aaron G., Liu, Weimin, Li, Yingying, Heisel, Sara E., Connell, Andrew Jesse, Ndjango, Jean-Bosco N., Bertolani, Paco, Hart, John A., Hart, Terese B., Sanz, Crickette M., Morgan, David B., Peeters, Martine, Sharp, Paul M., Hahn, Beatrice H., and Parham, Peter

Published
2023
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4. Recommendations for measuring HIV reservoir size in cure-directed clinical trials.

Author

Abdel-Mohsen, Mohamed, Richman, Douglas, Siliciano, Robert F, Nussenzweig, Michel C, Howell, Bonnie J, Martinez-Picado, Javier, Chomont, Nicolas, Bar, Katharine J, Yu, Xu G, Lichterfeld, Mathias, Alcami, Jose, Hazuda, Daria, Bushman, Frederic, Siliciano, Janet D, Betts, Michael R, Spivak, Adam M, Planelles, Vicente, Hahn, Beatrice H, Smith, Davey M, Ho, Ya-Chi, Buzon, Maria J, Gaebler, Christian, Paiardini, Mirko, Li, Qingsheng, Estes, Jacob D, Hope, Thomas J, Kostman, Jay, Mounzer, Karam, Caskey, Marina, Fox, Lawrence, Frank, Ian, Riley, James L, Tebas, Pablo, Montaner, Luis J, and BEAT-HIV Delaney Collaboratory to Cure HIV-1 infection

Subjects
BEAT-HIV Delaney Collaboratory to Cure HIV-1 infection, Medical and Health Sciences, Immunology
Abstract

Therapeutic strategies are being clinically tested either to eradicate latent HIV reservoirs or to achieve virologic control in the absence of antiretroviral therapy. Attaining this goal will require a consensus on how best to measure the numbers of persistently infected cells with the potential to cause viral rebound after antiretroviral-therapy cessation in assessing the results of cure-directed strategies in vivo. Current measurements assess various aspects of the HIV provirus and its functionality and produce divergent results. Here, we provide recommendations from the BEAT-HIV Martin Delaney Collaboratory on which viral measurements should be prioritized in HIV-cure-directed clinical trials.

Published
2020

5. Evasion of cGAS and TRIM5 defines pandemic HIV

Author

Zuliani-Alvarez, Lorena, Govasli, Morten L., Rasaiyaah, Jane, Monit, Chris, Perry, Stephen O., Sumner, Rebecca P., McAlpine-Scott, Simon, Dickson, Claire, Rifat Faysal, K. M., Hilditch, Laura, Miles, Richard J., Bibollet-Ruche, Frederic, Hahn, Beatrice H., Boecking, Till, Pinotsis, Nikos, James, Leo C., Jacques, David A., and Towers, Greg J.

Published
2022
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6. Small CD4 mimetics sensitize HIV-1-infected macrophages to antibody-dependent cellular cytotoxicity

Author

Laumaea, Annemarie, Marchitto, Lorie, Ding, Shilei, Beaudoin-Bussières, Guillaume, Prévost, Jérémie, Gasser, Romain, Chatterjee, Debashree, Gendron-Lepage, Gabrielle, Medjahed, Halima, Chen, Hung-Ching, Smith, Amos B., III, Ding, Haitao, Kappes, John C., Hahn, Beatrice H., Kirchhoff, Frank, Richard, Jonathan, Duerr, Ralf, and Finzi, Andrés

Published
2023
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7. HIV-1 Vpu restricts Fc-mediated effector functions in vivo

Author

Prévost, Jérémie, Anand, Sai Priya, Rajashekar, Jyothi Krishnaswamy, Zhu, Li, Richard, Jonathan, Goyette, Guillaume, Medjahed, Halima, Gendron-Lepage, Gabrielle, Chen, Hung-Ching, Chen, Yaozong, Horwitz, Joshua A., Grunst, Michael W., Zolla-Pazner, Susan, Haynes, Barton F., Burton, Dennis R., Flavell, Richard A., Kirchhoff, Frank, Hahn, Beatrice H., Smith, Amos B., III, Pazgier, Marzena, Nussenzweig, Michel C., Kumar, Priti, and Finzi, Andrés

Published
2022
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8. The ecology and epidemiology of malaria parasitism in wild chimpanzee reservoirs

Author

Scully, Erik J., Liu, Weimin, Li, Yingying, Ndjango, Jean-Bosco N., Peeters, Martine, Kamenya, Shadrack, Pusey, Anne E., Lonsdorf, Elizabeth V., Sanz, Crickette M., Morgan, David B., Piel, Alex K., Stewart, Fiona A., Gonder, Mary K., Simmons, Nicole, Asiimwe, Caroline, Zuberbühler, Klaus, Koops, Kathelijne, Chapman, Colin A., Chancellor, Rebecca, Rundus, Aaron, Huffman, Michael A., Wolfe, Nathan D., Duraisingh, Manoj T., Hahn, Beatrice H., and Wrangham, Richard W.

Published
2022
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11. Robust and durable serological response following pediatric SARS-CoV-2 infection

Author

Renk, Hanna, Dulovic, Alex, Seidel, Alina, Becker, Matthias, Fabricius, Dorit, Zernickel, Maria, Junker, Daniel, Groß, Rüdiger, Müller, Janis, Hilger, Alexander, Bode, Sebastian F. N., Fritsch, Linus, Frieh, Pauline, Haddad, Anneke, Görne, Tessa, Remppis, Jonathan, Ganzemueller, Tina, Dietz, Andrea, Huzly, Daniela, Hengel, Hartmut, Kaier, Klaus, Weber, Susanne, Jacobsen, Eva-Maria, Kaiser, Philipp D., Traenkle, Bjoern, Rothbauer, Ulrich, Stich, Maximilian, Tönshoff, Burkhard, Hoffmann, Georg F., Müller, Barbara, Ludwig, Carolin, Jahrsdörfer, Bernd, Schrezenmeier, Hubert, Peter, Andreas, Hörber, Sebastian, Iftner, Thomas, Münch, Jan, Stamminger, Thomas, Groß, Hans-Jürgen, Wolkewitz, Martin, Engel, Corinna, Liu, Weimin, Rizzi, Marta, Hahn, Beatrice H., Henneke, Philipp, Franz, Axel R., Debatin, Klaus-Michael, Schneiderhan-Marra, Nicole, Janda, Ales, and Elling, Roland

Published
2022
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12. CD4 receptor diversity represents an ancient protection mechanism against primate lentiviruses

Author

Russell, Ronnie M., Bibollet-Ruche, Frederic, Liu, Weimin, Sherrill-Mix, Scott, Li, Yingying, Connell, Jesse, Loy, Dorothy E., Trimboli, Stephanie, Smith, Andrew G., Avitto, Alexa N., Gondim, Marcos V. P., Plenderleith, Lindsey J., Wetzel, Katherine S., Collman, Ronald G., Ayouba, Ahidjo, Esteban, Amandine, Peeters, Martine, Kohler, William J., Miller, Richard A., François-Souquiere, Sandrine, Switzer, William M., Hirsch, Vanessa M., Marx, Preston A., Piel, Alex K., Stewart, Fiona A., Georgiev, Alexander V., Sommer, Volker, Bertolani, Paco, Hart, John A., Hart, Terese B., Shaw, George M., Sharp, Paul M., and Hahn, Beatrice H.

Published
2021

13. Exposure of progressive immune dysfunction by SARS-CoV-2 mRNA vaccination in patients with chronic lymphocytic leukemia: A prospective cohort study

Author

Qin, Kai, Honjo, Kazuhito, Sherrill-Mix, Scott, Liu, Weimin, Stoltz, Regina M., Oman, Allisa K., Hall, Lucinda A., Li, Ran, Sterrett, Sarah, Frederick, Ellen R., Lancaster, Jeffrey R., Narkhede, Mayur, Mehta, Amitkumar, Ogunsile, Foluso J., Patel, Rima B., Ketas, Thomas J., Cruz Portillo, Victor M., Cupo, Albert, Larimer, Benjamin M., Bansal, Anju, Goepfert, Paul A., Hahn, Beatrice H., and Davis, Randall S.

Subjects
Aged patients -- Care and treatment, Messenger RNA -- Analysis, Enzyme-linked immunosorbent assay -- Analysis, Antigens -- Testing, Chronic lymphocytic leukemia -- Diagnosis -- Care and treatment, Biological sciences
Abstract

Background Patients with chronic lymphocytic leukemia (CLL) have reduced seroconversion rates and lower binding antibody (Ab) and neutralizing antibody (NAb) titers than healthy individuals following Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) mRNA vaccination. Here, we dissected vaccine-mediated humoral and cellular responses to understand the mechanisms underlying CLL-induced immune dysfunction. Methods and findings We performed a prospective observational study in SARS-CoV-2 infection-naïve CLL patients (n = 95) and healthy controls (n = 30) who were vaccinated between December 2020 and June 2021. Sixty-one CLL patients and 27 healthy controls received 2 doses of the Pfizer-BioNTech BNT162b2 vaccine, while 34 CLL patients and 3 healthy controls received 2 doses of the Moderna mRNA-1273 vaccine. The median time to analysis was 38 days (IQR, 27 to 83) for CLL patients and 36 days (IQR, 28 to 57) for healthy controls. Testing plasma samples for SARS-CoV-2 anti-spike and receptor-binding domain Abs by enzyme-linked immunosorbent assay (ELISA), we found that all healthy controls seroconverted to both antigens, while CLL patients had lower response rates (68% and 54%) as well as lower median titers (23-fold and 30-fold; both p 23-fold and >17-fold lower median NAb titers (both p 2.4 mg/L), prior therapy, anti-CD20 immunotherapy ( Conclusions CLL pathogenesis is characterized by a progressive loss of adaptive immune functions, including in most treatment-naïve patients, with preexisting memory being preserved longer than the capacity to mount responses to new antigens. In addition, higher NAb titers and response rates identify mRNA-1273 as a superior vaccine for CLL patients., Author(s): Kai Qin 1, Kazuhito Honjo 1, Scott Sherrill-Mix 2, Weimin Liu 2, Regina M. Stoltz 2, Allisa K. Oman 1, Lucinda A. Hall 3, Ran Li 1, Sarah Sterrett [...]

Published
2023
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15. HLA-C downregulation by HIV-1 adapts to host HLA genotype.

Author

Bachtel, Nathaniel D, Umviligihozo, Gisele, Pickering, Suzanne, Mota, Talia M, Liang, Hua, Del Prete, Gregory Q, Chatterjee, Pramita, Lee, Guinevere Q, Thomas, Rasmi, Brockman, Mark A, Neil, Stuart, Carrington, Mary, Bwana, Bosco, Bangsberg, David R, Martin, Jeffrey N, Kallas, Esper G, Donini, Camila S, Cerqueira, Natalia B, O'Doherty, Una T, Hahn, Beatrice H, Jones, R Brad, Brumme, Zabrina L, Nixon, Douglas F, and Apps, Richard

Subjects
Humans, HIV-1, HIV Infections, HLA-C Antigens, Disease Reservoirs, Down-Regulation, Amino Acid Sequence, Genotype, Human Immunodeficiency Virus Proteins, Viral Regulatory and Accessory Proteins, Host-Pathogen Interactions, Genetic Variation, Immune Evasion, Microbiology, Immunology, Medical Microbiology, Virology
Abstract

HIV-1 can downregulate HLA-C on infected cells, using the viral protein Vpu, and the magnitude of this downregulation varies widely between primary HIV-1 variants. The selection pressures that result in viral downregulation of HLA-C in some individuals, but preservation of surface HLA-C in others are not clear. To better understand viral immune evasion targeting HLA-C, we have characterized HLA-C downregulation by a range of primary HIV-1 viruses. 128 replication competent viral isolates from 19 individuals with effective anti-retroviral therapy, show that a substantial minority of individuals harbor latent reservoir virus which strongly downregulates HLA-C. Untreated infections display no change in HLA-C downregulation during the first 6 months of infection, but variation between viral quasispecies can be detected in chronic infection. Vpu molecules cloned from plasma of 195 treatment naïve individuals in chronic infection demonstrate that downregulation of HLA-C adapts to host HLA genotype. HLA-C alleles differ in the pressure they exert for downregulation, and individuals with higher levels of HLA-C expression favor greater viral downregulation of HLA-C. Studies of primary and mutant molecules identify 5 residues in the transmembrane region of Vpu, and 4 residues in the transmembrane domain of HLA-C, which determine interactions between Vpu and HLA. The observed adaptation of Vpu-mediated downregulation to host genotype indicates that HLA-C alleles differ in likelihood of mediating a CTL response that is subverted by viral downregulation, and that preservation of HLA-C expression is favored in the absence of these responses. Finding that latent reservoir viruses can downregulate HLA-C could have implications for HIV-1 cure therapy approaches in some individuals.

Published
2018

16. Predictors of Nonseroconversion after SARS-CoV-2 Infection

Author

Liu, Weimin, Russell, Ronnie M., Bibollet-Ruche, Frederic, Skelly, Ashwin N., Sherrill-Mix, Scott, Freeman, Drew A., Stoltz, Regina, Lindemuth, Emily, Lee, Fang-Hua, Sterrett, Sarah, Bar, Katharine J., Erdmann, Nathaniel, Gouma, Sigrid, Hensley, Scott E., Ketas, Thomas, Cupo, Albert, Portillo, Victor M. Cruz, Moore, John P., Bieniasz, Paul D., Hatziioannou, Theodora, Massey, Greer, Minyard, Mary-Beth, Saag, Michael S., Davis, Randall S., Shaw, George M., Britt, William J., Leal, Sixto M., Jr., Goepfert, Paul, and Hahn, Beatrice H.

Subjects
Antigen-antibody reactions -- Research, Immunological research, Health
Abstract

Coronavirus disease (COVID-19) is typically diagnosed by reverse transcription PCR (RT-PCR) amplification of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA from nasopharyngeal fluids (1). RT-PCR yields cycle threshold ([C.sub.t]) [...]

Published
2021
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17. Contribution of proteasome-catalyzed peptide cis -splicing to viral targeting by CD8⁺ T cells in HIV-1 infection

Author

Paes, Wayne, Leonov, German, Partridge, Thomas, Chikata, Takayuki, Murakoshi, Hayato, Frangou, Anna, Brackenridge, Simon, Nicastri, Annalisa, Smith, Andrew G., Learn, Gerald H., Li, Yingying, Parker, Robert, Oka, Shinichi, Pellegrino, Pierre, Williams, Ian, Haynes, Barton F., McMichael, Andrew J., Shaw, George M., Hahn, Beatrice H., Takiguchi, Masafumi, Ternette, Nicola, and Borrow, Persephone

Published
2019

19. Selective Whole-Genome Amplification Is a Robust Method That Enables Scalable Whole-Genome Sequencing of Plasmodium vivax from Unprocessed Clinical Samples

Author

Cowell, Annie N, Loy, Dorothy E, Sundararaman, Sesh A, Valdivia, Hugo, Fisch, Kathleen, Lescano, Andres G, Baldeviano, G Christian, Durand, Salomon, Gerbasi, Vince, Sutherland, Colin J, Nolder, Debbie, Vinetz, Joseph M, Hahn, Beatrice H, and Winzeler, Elizabeth A

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Microbiology, Clinical Sciences, Medical Microbiology, Emerging Infectious Diseases, Antimicrobial Resistance, Clinical Research, Biodefense, Infectious Diseases, Rare Diseases, Vector-Borne Diseases, Genetics, Biotechnology, Human Genome, Malaria, 2.2 Factors relating to the physical environment, Infection, Good Health and Well Being, Blood, Humans, Malaria, Vivax, Nucleic Acid Amplification Techniques, Peru, Plasmodium vivax, Sequence Analysis, DNA, Biochemistry and cell biology, Medical microbiology
Abstract

Whole-genome sequencing (WGS) of microbial pathogens from clinical samples is a highly sensitive tool used to gain a deeper understanding of the biology, epidemiology, and drug resistance mechanisms of many infections. However, WGS of organisms which exhibit low densities in their hosts is challenging due to high levels of host genomic DNA (gDNA), which leads to very low coverage of the microbial genome. WGS of Plasmodium vivax, the most widely distributed form of malaria, is especially difficult because of low parasite densities and the lack of an ex vivo culture system. Current techniques used to enrich P. vivax DNA from clinical samples require significant resources or are not consistently effective. Here, we demonstrate that selective whole-genome amplification (SWGA) can enrich P. vivax gDNA from unprocessed human blood samples and dried blood spots for high-quality WGS, allowing genetic characterization of isolates that would otherwise have been prohibitively expensive or impossible to sequence. We achieved an average genome coverage of 24×, with up to 95% of the P. vivax core genome covered by ≥5 reads. The single-nucleotide polymorphism (SNP) characteristics and drug resistance mutations seen were consistent with those of other P. vivax sequences from a similar region in Peru, demonstrating that SWGA produces high-quality sequences for downstream analysis. SWGA is a robust tool that will enable efficient, cost-effective WGS of P. vivax isolates from clinical samples that can be applied to other neglected microbial pathogens.ImportanceMalaria is a disease caused by Plasmodium parasites that caused 214 million symptomatic cases and 438,000 deaths in 2015. Plasmodium vivax is the most widely distributed species, causing the majority of malaria infections outside sub-Saharan Africa. Whole-genome sequencing (WGS) of Plasmodium parasites from clinical samples has revealed important insights into the epidemiology and mechanisms of drug resistance of malaria. However, WGS of P. vivax is challenging due to low parasite levels in humans and the lack of a routine system to culture the parasites. Selective whole-genome amplification (SWGA) preferentially amplifies the genomes of pathogens from mixtures of target and host gDNA. Here, we demonstrate that SWGA is a simple, robust method that can be used to enrich P. vivax genomic DNA (gDNA) from unprocessed human blood samples and dried blood spots for cost-effective, high-quality WGS.

Published
2017

20. Paired quantitative and qualitative assessment of the replication-competent HIV-1 reservoir and comparison with integrated proviral DNA

Author

Lorenzi, Julio CC, Cohen, Yehuda Z, Cohn, Lillian B, Kreider, Edward F, Barton, John P, Learn, Gerald H, Oliveira, Thiago, Lavine, Christy L, Horwitz, Joshua A, Settler, Allison, Jankovic, Mila, Seaman, Michael S, Chakraborty, Arup K, Hahn, Beatrice H, Caskey, Marina, and Nussenzweig, Michel C

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, HIV/AIDS, Aetiology, 2.2 Factors relating to the physical environment, Infection, Good Health and Well Being, HIV, reservoir, replication-competent, culture, method
Abstract

HIV-1-infected individuals harbor a latent reservoir of infected CD4+ T cells that is not eradicated by antiretroviral therapy (ART). This reservoir presents the greatest barrier to an HIV-1 cure and has remained difficult to characterize, in part, because the vast majority of integrated sequences are defective and incapable of reactivation. To characterize the replication-competent reservoir, we have combined two techniques, quantitative viral outgrowth and qualitative sequence analysis of clonal outgrowth viruses. Leukapheresis samples from four fully ART-suppressed, chronically infected individuals were assayed at two time points separated by a 4- to 6-mo interval. Overall, 54% of the viruses emerging from the latent reservoir showed gp160 env sequences that were identical to at least one other virus. Moreover, 43% of the env sequences from viruses emerging from the reservoir were part of identical groups at the two time points. Groups of identical expanded sequences made up 54% of proviral DNA, and, as might be expected, the sequences of replication-competent viruses in the active reservoir showed limited overlap with integrated proviral DNA, most of which is known to represent defective viruses. Finally, there was an inverse correlation between proviral DNA clone size and the probability of reactivation, suggesting that replication-competent viruses are less likely to be found among highly expanded provirus-containing cell clones.

Published
2016

21. Longitudinal Antigenic Sequences and Sites from Intra-Host Evolution (LASSIE) Identifies Immune-Selected HIV Variants

Author

Hraber, Peter, Korber, Bette, Wagh, Kshitij, Giorgi, Elena E., Bhattacharya, Tanmoy, Gnanakaran, S., Lapedes, Alan S., Learn, Gerald H., Kreider, Edward F., Li, Yingying, Shaw, George M., Hahn, Beatrice H., Montefiori, David C., Alam, S. Munir, Bonsignori, Mattia, Moody, M. Anthony, Liao, Hua-Xin, Gao, Feng, and Haynes, Barton F.

Subjects
Quantitative Biology - Populations and Evolution, Quantitative Biology - Quantitative Methods
Abstract

Within-host genetic sequencing from samples collected over time provides a dynamic view of how viruses evade host immunity. Immune-driven mutations might stimulate neutralization breadth by selecting antibodies adapted to cycles of immune escape that generate within-subject epitope diversity. Comprehensive identification of immune-escape mutations is experimentally and computationally challenging. With current technology, many more viral sequences can readily be obtained than can be tested for binding and neutralization, making down-selection necessary. Typically, this is done manually, by picking variants that represent different time-points and branches on a phylogenetic tree. Such strategies are likely to miss many relevant mutations and combinations of mutations, and to be redundant for other mutations. Longitudinal Antigenic Sequences and Sites from Intrahost Evolution (LASSIE) uses transmitted-founder loss to identify virus "hot-spots" under putative immune selection and chooses sequences that represent recurrent mutations in selected sites. LASSIE favors earliest sequences in which mutations arise. With well-characterized longitudinal Env sequences, we confirmed selected sites were concentrated in antibody contacts and selected sequences represented diverse antigenic phenotypes. Practical applications include rapidly identifying immune targets under selective pressure within a subject, selecting minimal sets of reagents for immunological assays that characterize evolving antibody responses, and for immunogens in polyvalent "cocktail" vaccines., Comment: 73 pages, 10 figures, 8 supplemental figures; 18 full-resolution figures appear at the end of the manuscript. Presented at 22nd International Workshop on HIV Dynamics and Evolution, Budapest, May 2015

Published
2015

22. CD4 receptor diversity in chimpanzees protects against SIV infection

Author

Bibollet-Ruche, Frederic, Russell, Ronnie M., Liu, Weimin, Stewart-Jones, Guillaume B. E., Sherrill-Mix, Scott, Li, Yingying, Learn, Gerald H., Smith, Andrew G., Gondim, Marcos V. P., Plenderleith, Lindsey J., Decker, Julie M., Easlick, Juliet L., Wetzel, Katherine S., Collman, Ronald G., Ding, Shilei, Finzi, Andrés, Ayouba, Ahidjo, Peeters, Martine, Leendertz, Fabian H., van Schijndel, Joost, Goedmakers, Annemarie, Ton, Els, Boesch, Christophe, Kuehl, Hjalmar, Arandjelovic, Mimi, Dieguez, Paula, Murai, Mizuki, Colin, Christelle, Koops, Kathelijne, Speede, Sheri, Gonder, Mary K., Muller, Martin N., Sanz, Crickette M., Morgan, David B., Atencia, Rebecca, Cox, Debby, Piel, Alex K., Stewart, Fiona A., Ndjango, Jean-Bosco N., Mjungu, Deus, Lonsdorf, Elizabeth V., Pusey, Anne E., Kwong, Peter D., Sharp, Paul M., Shaw, George M., and Hahn, Beatrice H.

Published
2019

24. The Role of the Antiviral APOBEC3 Gene Family in Protecting Chimpanzees against Lentiviruses from Monkeys

Author

Etienne, Lucie, Bibollet-Ruche, Frederic, Sudmant, Peter H, Wu, Lily I, Hahn, Beatrice H, and Emerman, Michael

Subjects
Genetics, Infection, Animals, Blotting, Western, CD4-Positive T-Lymphocytes, Cytidine Deaminase, Genes, vif, Haplorhini, Lentivirus, Lentivirus Infections, Molecular Sequence Data, Pan troglodytes, Phylogeny, Polymerase Chain Reaction, Simian Immunodeficiency Virus, Simian immunodeficiency virus, Microbiology, Immunology, Medical Microbiology, Virology
Abstract

Cross-species transmissions of viruses from animals to humans are at the origin of major human pathogenic viruses. While the role of ecological and epidemiological factors in the emergence of new pathogens is well documented, the importance of host factors is often unknown. Chimpanzees are the closest relatives of humans and the animal reservoir at the origin of the human AIDS pandemic. However, despite being regularly exposed to monkey lentiviruses through hunting, chimpanzees are naturally infected by only a single simian immunodeficiency virus, SIVcpz. Here, we asked why chimpanzees appear to be protected against the successful emergence of other SIVs. In particular, we investigated the role of the chimpanzee APOBEC3 genes in providing a barrier to infection by most monkey lentiviruses. We found that most SIV Vifs, including Vif from SIVwrc infecting western-red colobus, the chimpanzee's main monkey prey in West Africa, could not antagonize chimpanzee APOBEC3G. Moreover, chimpanzee APOBEC3D, as well as APOBEC3F and APOBEC3H, provided additional protection against SIV Vif antagonism. Consequently, lentiviral replication in primary chimpanzee CD4(+) T cells was dependent on the presence of a lentiviral vif gene that could antagonize chimpanzee APOBEC3s. Finally, by identifying and functionally characterizing several APOBEC3 gene polymorphisms in both common chimpanzees and bonobos, we found that these ape populations encode APOBEC3 proteins that are uniformly resistant to antagonism by monkey lentiviruses.

Published
2015

25. Extreme selective sweeps independently targeted the X chromosomes of the great apes

Author

Nam, Kiwoong, Munch, Kasper, Hobolth, Asger, Dutheil, Julien Yann, Veeramah, Krishna R, Woerner, August E, Hammer, Michael F, Mailund, Thomas, Schierup, Mikkel Heide, Prado-Martinez, Javier, Sudmant, Peter H, Kidd, Jeffrey M, Li, Heng, Kelley, Joanna L, Lorente-Galdos, Belen, O’Connor, Timothy D, Santpere, Gabriel, Cagan, Alexander, Theunert, Christoph, Casals, Ferran, Laayouni, Hafid, Halager, Anders E, Malig, Maika, Hernandez-Rodriguez, Jessica, Hernando-Herraez, Irene, Prüfer, Kay, Pybus, Marc, Johnstone, Laurel, Lachmann, Michael, Alkan, Can, Twigg, Dorina, Petit, Natalia, Baker, Carl, Hormozdiari, Fereydoun, Fernandez-Callejo, Marcos, Dabad, Marc, Wilson, Michael L, Stevison, Laurie, Camprubí, Cristina, Carvalho, Tiago, Ruiz-Herrera, Aurora, Vives, Laura, Mele, Marta, Abello, Teresa, Kondova, Ivanela, Bontrop, Ronald E, Pusey, Anne, Lankester, Felix, Kiyang, John A, Bergl, Richard A, Lonsdorf, Elizabeth, Myers, Simon, Ventura, Mario, Gagneux, Pascal, Comas, David, Siegismund, Hans, Blanc, Julie, Agueda-Calpena, Lidia, Gut, Marta, Fulton, Lucinda, Tishkoff, Sarah A, Mullikin, James C, Wilson, Richard K, Gut, Ivo G, Gonder, Mary Katherine, Ryder, Oliver A, Hahn, Beatrice H, Navarro, Arcadi, Akey, Joshua M, Bertranpetit, Jaume, Reich, David, Schierup, Mikkel H, Hvilsom, Christina, Andrés, Aida M, Wall, Jeffrey D, Bustamante, Carlos D, Eichler, Evan E, and Marques-Bonet, Tomas

Subjects
Human Genome, Genetics, Animals, Computational Biology, Databases, Genetic, Genetic Variation, Genetics, Population, Hominidae, Models, Genetic, Polymorphism, Genetic, Selection, Genetic, Species Specificity, X Chromosome, Great Ape Genome Diversity Project, X-chromosome evolution, ampliconic genes, great apes, meiotic drive, selective sweeps
Abstract

The unique inheritance pattern of the X chromosome exposes it to natural selection in a way that is different from that of the autosomes, potentially resulting in accelerated evolution. We perform a comparative analysis of X chromosome polymorphism in 10 great ape species, including humans. In most species, we identify striking megabase-wide regions, where nucleotide diversity is less than 20% of the chromosomal average. Such regions are found exclusively on the X chromosome. The regions overlap partially among species, suggesting that the underlying targets are partly shared among species. The regions have higher proportions of singleton SNPs, higher levels of population differentiation, and a higher nonsynonymous-to-synonymous substitution ratio than the rest of the X chromosome. We show that the extent to which diversity is reduced is incompatible with direct selection or the action of background selection and soft selective sweeps alone, and therefore, we suggest that very strong selective sweeps have independently targeted these specific regions in several species. The only genomic feature that we can identify as strongly associated with loss of diversity is the location of testis-expressed ampliconic genes, which also have reduced diversity around them. We hypothesize that these genes may be responsible for selective sweeps in the form of meiotic drive caused by an intragenomic conflict in male meiosis.

Published
2015

26. Evolutionary history of human Plasmodium vivax revealed by genome-wide analyses of related ape parasites

Author

Loy, Dorothy E., Plenderleith, Lindsey J., Sundararaman, Sesh A., Liu, Weimin, Gruszczyk, Jakub, Chen, Yi-Jun, Trimboli, Stephanie, Learn, Gerald H., MacLean, Oscar A., Morgan, Alex L. K., Li, Yingying, Avitto, Alexa N., Giles, Jasmin, Calvignac-Spencer, Sébastien, Sachse, Andreas, Leendertz, Fabian H., Speede, Sheri, Ayouba, Ahidjo, Peeters, Martine, Rayner, Julian C., Tham, Wai-Hong, Sharp, Paul M., and Hahn, Beatrice H.

Published
2018

29. Great ape genetic diversity and population history.

Author

Prado-Martinez, Javier, Sudmant, Peter H, Kidd, Jeffrey M, Li, Heng, Kelley, Joanna L, Lorente-Galdos, Belen, Veeramah, Krishna R, Woerner, August E, O'Connor, Timothy D, Santpere, Gabriel, Cagan, Alexander, Theunert, Christoph, Casals, Ferran, Laayouni, Hafid, Munch, Kasper, Hobolth, Asger, Halager, Anders E, Malig, Maika, Hernandez-Rodriguez, Jessica, Hernando-Herraez, Irene, Prüfer, Kay, Pybus, Marc, Johnstone, Laurel, Lachmann, Michael, Alkan, Can, Twigg, Dorina, Petit, Natalia, Baker, Carl, Hormozdiari, Fereydoun, Fernandez-Callejo, Marcos, Dabad, Marc, Wilson, Michael L, Stevison, Laurie, Camprubí, Cristina, Carvalho, Tiago, Ruiz-Herrera, Aurora, Vives, Laura, Mele, Marta, Abello, Teresa, Kondova, Ivanela, Bontrop, Ronald E, Pusey, Anne, Lankester, Felix, Kiyang, John A, Bergl, Richard A, Lonsdorf, Elizabeth, Myers, Simon, Ventura, Mario, Gagneux, Pascal, Comas, David, Siegismund, Hans, Blanc, Julie, Agueda-Calpena, Lidia, Gut, Marta, Fulton, Lucinda, Tishkoff, Sarah A, Mullikin, James C, Wilson, Richard K, Gut, Ivo G, Gonder, Mary Katherine, Ryder, Oliver A, Hahn, Beatrice H, Navarro, Arcadi, Akey, Joshua M, Bertranpetit, Jaume, Reich, David, Mailund, Thomas, Schierup, Mikkel H, Hvilsom, Christina, Andrés, Aida M, Wall, Jeffrey D, Bustamante, Carlos D, Hammer, Michael F, Eichler, Evan E, and Marques-Bonet, Tomas

Subjects
Animals, Animals, Wild, Animals, Zoo, Hominidae, Gorilla gorilla, Humans, Pan paniscus, Pan troglodytes, Inbreeding, Genetics, Population, Population Density, Evolution, Molecular, Phylogeny, Polymorphism, Single Nucleotide, Genome, Africa, Asia, Southeastern, Gene Flow, Genetic Variation, General Science & Technology
Abstract

Most great ape genetic variation remains uncharacterized; however, its study is critical for understanding population history, recombination, selection and susceptibility to disease. Here we sequence to high coverage a total of 79 wild- and captive-born individuals representing all six great ape species and seven subspecies and report 88.8 million single nucleotide polymorphisms. Our analysis provides support for genetically distinct populations within each species, signals of gene flow, and the split of common chimpanzees into two distinct groups: Nigeria-Cameroon/western and central/eastern populations. We find extensive inbreeding in almost all wild populations, with eastern gorillas being the most extreme. Inferred effective population sizes have varied radically over time in different lineages and this appears to have a profound effect on the genetic diversity at, or close to, genes in almost all species. We discover and assign 1,982 loss-of-function variants throughout the human and great ape lineages, determining that the rate of gene loss has not been different in the human branch compared to other internal branches in the great ape phylogeny. This comprehensive catalogue of great ape genome diversity provides a framework for understanding evolution and a resource for more effective management of wild and captive great ape populations.

Published
2013

31. Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1

Author

Keele, Brandon F., Van Heuverswyn, Fran, Li, Yingying, Bailes, Elizabeth, Takehisa, Jun, Santiago, Mario L., Bibollet-Ruche, Frederic, Chen, Yalu, Wain, Louise V., Liegeois, Florian, Loul, Severin, Ngole, Eitel Mpoudi, Bienvenue, Yanga, Delaporte, Eric, Sharp, Paul M., Shaw, George M., Peeters, Martine, and Hahn, Beatrice H.

Published
2006

32. Semen-mediated enhancement of HIV infection is donor-dependent and correlates with the levels of SEVI

Author

Kim, Kyeong-Ae, Yolamanova, Maral, Zirafi, Onofrio, Roan, Nadia R, Staendker, Ludger, Forssmann, Wolf-Georg, Burgener, Adam, Dejucq-Rainsford, Nathalie, Hahn, Beatrice H, Shaw, George M, Greene, Warner C, Kirchhoff, Frank, and Münch, Jan

Abstract

Abstract Background HIV-1 is usually transmitted in the presence of semen. We have shown that semen boosts HIV-1 infection and contains fragments of prostatic acid phosphatase (PAP) forming amyloid aggregates termed SEVI (semen-derived enhancer of viral infection) that promote virion attachment to target cells. Despite its importance for the global spread of HIV-1, however, the effect of semen on virus infection is controversial. Results Here, we established methods allowing the meaningful analysis of semen by minimizing its cytotoxic effects and partly recapitulating the conditions encountered during sexual HIV-1 transmission. We show that semen rapidly and effectively enhances the infectivity of HIV-1, HIV-2, and SIV. This enhancement occurs independently of the viral genotype and coreceptor tropism as well as the virus producer and target cell type. Semen-mediated enhancement of HIV-1 infection was also observed under acidic pH conditions and in the presence of vaginal fluid. We further show that the potency of semen in boosting HIV-1 infection is donor dependent and correlates with the levels of SEVI. Conclusions Our results show that semen strongly enhances the infectivity of HIV-1 and other primate lentiviruses and that SEVI contributes to this effect. Thus, SEVI may play an important role in the sexual transmission of HIV-1 and addition of SEVI inhibitors to microbicides may improve their efficacy.

Published
2010

33. Support for the RV144 HIV Vaccine Trial

Author

Belshe, Robert, Franchini, Genoveffa, Girard, Marc P., Gotch, Frances, Kaleebu, Pontiano, Marthas, Marta L., McChesney, Michael B., McCullough, Rose, Mhalu, Fred, Salmon-Ceron, Dominique, Sekaly, Rafick-Pierre, Van Rompay, Koen, Verrier, Bernard, Wahren, Britta, Weissenbacher, Mercedes, Burton, Dennis R., Desrosiers, Ronald C., Doms, Robert W., Feinberg, Mark B., Hahn, Beatrice H., Hoxie, James A., Hunter, Eric, Landay, Alan L., Lederman, Michael M., Lieberman, Judy, McCune, Joseph M., Moore, John P., Nathanson, Neal, Picker, Louis, Richman, Douglas D., Rinaldo, Charles R., Stevenson, Mario, Watkins, David I., Wolinsky, Steven M., Zack, Jerome A., and Gallo, Robert C.

Published
2004

35. Resistance to type 1 interferons is a major determinant of HIV-1 transmission fitness

Author

Iyer, Shilpa S., Bibollet-Ruche, Frederic, Sherrill-Mix, Scott, Learn, Gerald H., Plenderleith, Lindsey, Smith, Andrew G., Barbian, Hannah J., Russell, Ronnie M., Gondim, Marcos V. P., Bahari, Catherine Y., Shaw, Christiana M., Li, Yingying, Decker, Timothy, Haynes, Barton F., Shaw, George M., Sharp, Paul M., Borrow, Persephone, and Hahn, Beatrice H.

Published
2017

36. Single-cell transcriptomics identifies prothymosin α restriction of HIV-1 in vivo

Author

Geretz, Aviva, primary, Ehrenberg, Philip K., additional, Clifford, Robert J., additional, Laliberté, Alexandre, additional, Prelli Bozzo, Caterina, additional, Eiser, Daina, additional, Kundu, Gautam, additional, Yum, Lauren K., additional, Apps, Richard, additional, Creegan, Matthew, additional, Gunady, Mohamed, additional, Shangguan, Shida, additional, Sanders-Buell, Eric, additional, Sacdalan, Carlo, additional, Phanuphak, Nittaya, additional, Tovanabutra, Sodsai, additional, Russell, Ronnie M., additional, Bibollet-Ruche, Frederic, additional, Robb, Merlin L., additional, Michael, Nelson L., additional, Ake, Julie A., additional, Vasan, Sandhya, additional, Hsu, Denise C., additional, Hahn, Beatrice H., additional, Kirchhoff, Frank, additional, and Thomas, Rasmi, additional

Published
2023
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38. Impact of HIV-1 Vpu-mediated downregulation of CD48 on NK-cell-mediated antibody-dependent cellular cytotoxicity

Author

Marchitto, Lorie, primary, Benlarbi, Mehdi, additional, Prévost, Jérémie, additional, Laumaea, Annemarie, additional, Descôteaux-Dinelle, Jade, additional, Medjahed, Halima, additional, Bourassa, Catherine, additional, Gendron-Lepage, Gabrielle, additional, Kirchhoff, Frank, additional, Sauter, Daniel, additional, Hahn, Beatrice H., additional, Finzi, Andrés, additional, and Richard, Jonathan, additional

Published
2023
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39. Reproductive inequality among males in the genusPan

Author

Mouginot, Maud, primary, Cheng, Leveda, additional, Wilson, Michael L., additional, Feldblum, Joseph T., additional, Städele, Veronika, additional, Wroblewski, Emily E., additional, Vigilant, Linda, additional, Hahn, Beatrice H., additional, Li, Yingying, additional, Gilby, Ian C., additional, Pusey, Anne E., additional, and Surbeck, Martin, additional

Published
2023
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40. Barriers to chimpanzee gene flow at the south‐east edge of their distribution

Author

Bonnin, Noémie, primary, Piel, Alex K., additional, Brown, Richard P., additional, Li, Yingying, additional, Connell, Andrew Jesse, additional, Avitto, Alexa N., additional, Boubli, Jean P., additional, Chitayat, Adrienne, additional, Giles, Jasmin, additional, Gundlapally, Madhurima S., additional, Lipende, Iddi, additional, Lonsdorf, Elizabeth V., additional, Mjungu, Deus, additional, Mwacha, Dismas, additional, Pintea, Lilian, additional, Pusey, Anne E., additional, Raphael, Jane, additional, Wich, Serge A., additional, Wilson, Michael L., additional, Wroblewski, Emily E., additional, Hahn, Beatrice H., additional, and Stewart, Fiona A., additional

Published
2023
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41. Diversity Considerations in HIV-1 Vaccine Selection

Author

Gaschen, Brian, Taylor, Jesse, Yusim, Karina, Foley, Brian, Gao, Feng, Lang, Dorothy, Novitsky, Vladimir, Haynes, Barton, Hahn, Beatrice H., Bhattacharya, Tanmoy, and Korber, Bette

Published
2002

48. Sooty mangabey genome sequence provides insight into AIDS resistance in a natural SIV host

Author

Palesch, David, Bosinger, Steven E., Tharp, Gregory K., Vanderford, Thomas H., Paiardini, Mirko, Chahroudi, Ann, Johnson, Zachary P., Kirchhoff, Frank, Hahn, Beatrice H., Norgren, Robert B., Patel, Nirav B., Sodora, Donald L., Dawoud, Reem A., Stewart, Caro-Beth, Seepo, Sara M., Harris, R. Alan, Liu, Yue, Raveendran, Muthuswamy, Han, Yi, English, Adam, Thomas, Gregg W. C., Hahn, Matthew W., Pipes, Lenore, Mason, Christopher E., Muzny, Donna M., Gibbs, Richard A., Sauter, Daniel, Worley, Kim, Rogers, Jeffrey, and Silvestri, Guido

Subjects
Immunity (Physiology) -- Genetic aspects, Sooty mangabey -- Genetic aspects -- Health aspects, Simian immunodeficiency virus -- Health aspects -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): David Palesch [1]; Steven E. Bosinger [1, 2]; Gregory K. Tharp [1]; Thomas H. Vanderford [1]; Mirko Paiardini [1, 2]; Ann Chahroudi [1, 3]; Zachary P. Johnson [1]; Frank [...]

Published
2018
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49. Widespread extinctions of co-diversified primate gut bacterial symbionts from humans

Author

Sanders, Jon G., primary, Sprockett, Daniel D., additional, Li, Yingying, additional, Mjungu, Deus, additional, Lonsdorf, Elizabeth V., additional, Ndjango, Jean-Bosco N., additional, Georgiev, Alexander V., additional, Hart, John A., additional, Sanz, Crickette M., additional, Morgan, David B., additional, Peeters, Martine, additional, Hahn, Beatrice H., additional, and Moeller, Andrew H., additional

Published
2023
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