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2. Apobec-mediated retroviral hypermutation in vivo is dependent on mouse strain.

Author

Byun, Hyewon, Singh, Gurvani B., Xu, Wendy Kaichun, Das, Poulami, Reyes, Alejandro, Battenhouse, Anna, Wylie, Dennis C., Santiago, Mario L., Lozano, Mary M., and Dudley, Jaquelin P.

Subjects
MOUSE mammary tumor virus, CYTIDINE deaminase, GENE expression, NUCLEIC acids, KNOCKOUT mice
Abstract

Replication of the complex retrovirus mouse mammary tumor virus (MMTV) is antagonized by murine Apobec3 (mA3), a member of the Apobec family of cytidine deaminases. We have shown that MMTV-encoded Rem protein inhibits proviral mutagenesis by the Apobec enzyme, activation-induced cytidine deaminase (AID) during viral replication in BALB/c mice. To further study the role of Rem in vivo, we have infected C57BL/6 (B6) mice with a superantigen-independent lymphomagenic strain of MMTV (TBLV-WT) or a mutant strain that is defective in Rem and its cleavage product Rem-CT (TBLV-SD). Compared to BALB/c, B6 mice were more susceptible to TBLV infection and tumorigenesis. Furthermore, unlike MMTV, TBLV induced T-cell tumors in B6 μMT mice, which lack membrane-bound IgM and conventional B-2 cells. At limiting viral doses, loss of Rem expression in TBLV-SD-infected B6 mice accelerated tumorigenesis compared to TBLV-WT in either wild-type B6 or AID-knockout mice. Unlike BALB/c results, high-throughput sequencing indicated that proviral G-to-A or C-to-T mutations were unchanged regardless of Rem expression in B6 tumors. However, knockout of both AID and mA3 reduced G-to-A mutations. Ex vivo stimulation showed higher levels of mA3 relative to AID in B6 compared to BALB/c splenocytes, and effects of agonists differed in the two strains. RNA-Seq revealed increased transcripts related to growth factor and cytokine signaling in TBLV-SD-induced tumors relative to TBLV-WT-induced tumors, consistent with another Rem function. Thus, Rem-mediated effects on tumorigenesis in B6 mice are independent of Apobec-mediated proviral hypermutation. Author summary: Retroviruses cause lifelong infections resulting from their ability to thwart innate immunity. The Apobec family of cytidine deaminases are part of the innate immune response that recognizes and mutates foreign nucleic acids, including those from multiple viruses. Retroviral antagonists of Apobecs have been identified, including mouse mammary tumor virus (MMTV)-encoded Rem protein. Previous experiments have shown that Rem-null MMTV or closely related TBLV proviruses from BALB/c tumors accumulate G-to-A and C-to-T mutations typical of Apobecs compared to wild-type proviruses expressing Rem. The difference in mutations between Rem-expressing and non-expressing MMTV strains largely disappeared in mice lacking the Apobec family member, activation-induced cytidine deaminase (AID). These results suggested that Rem is an AID antagonist. In this study, we attempted to study AID-mediated mutations of TBLV proviruses lacking Rem expression obtained from tumors in C57BL/6 (B6) wild-type and AID-knockout backgrounds. Surprisingly, no differences in G-to-A mutations were observed in TBLV proviruses regardless of Rem expression, yet such mutations were significantly reduced in proviruses obtained from mA3/AID-double knockout mice relative to those from wild-type B6 or AID-knockout mice. Many cellular mRNAs involving the innate immune response, but not Apobecs, were elevated in the absence relative to the presence of Rem expression on the B6 AID-knockout background. These results revealed that Apobec-mediated mutagenesis is dependent on mouse strain and suggested a second means of Rem-dependent immune evasion. [ABSTRACT FROM AUTHOR]

Published
2024
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3. A compartmentalized type I interferon response in the gut during chronic HIV-1 infection is associated with immunopathogenesis

Author

Dillon, Stephanie M, Guo, Kejun, Austin, Gregory L, Gianella, Sara, Engen, Phillip A, Mutlu, Ece A, Losurdo, John, Swanson, Garth, Chakradeo, Prachi, Keshavarzian, Ali, Landay, Alan L, Santiago, Mario L, and Wilson, Cara C

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Genetics, Digestive Diseases, Infectious Diseases, Clinical Research, HIV/AIDS, Development of treatments and therapeutic interventions, Aetiology, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Infection, Good Health and Well Being, Adult, Biopsy, Colon, Cross-Sectional Studies, Female, Gene Expression Profiling, HIV Infections, Humans, Immunologic Factors, Interferon Type I, Intestinal Mucosa, Leukocytes, Mononuclear, Male, Middle Aged, Young Adult, gut, HIV-1 infection, interferon-stimulated genes, inflammation, mucosal immunology, type I interferon, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology, Biomedical and clinical sciences, Health sciences
Abstract

Objective(s)Type I interferon (IFN-I) responses confer both protective and pathogenic effects in persistent virus infections. IFN-I diversity, stage of infection and tissue compartment may account for this dichotomy. The gut is a major site of early HIV-1 replication and microbial translocation, but the nature of the IFN-I response in this compartment remains unclear.DesignSamples were obtained from two IRB-approved cross-sectional studies. The first study included individuals with chronic, untreated HIV-1 infection (n = 24) and age/sex-balanced uninfected controls (n = 14). The second study included antiretroviral-treated, HIV-1-infected individuals (n = 15) and uninfected controls (n = 15).MethodsThe expression of 12 IFNα subtypes, IFNβ and antiviral IFN-stimulated genes (ISGs) were quantified in peripheral blood mononuclear cells (PBMCs) and colon biopsies using real-time PCR and next-generation sequencing. In untreated HIV-1-infected individuals, associations between IFN-I responses and gut HIV-1 RNA levels as well as previously established measures of colonic and systemic immunological indices were determined.ResultsIFNα1, IFNα2, IFNα4, IFNα5 and IFNα8 were upregulated in PBMCs during untreated chronic HIV-1 infection, but IFNβ was undetectable. By contrast, IFNβ was upregulated and all IFNα subtypes were downregulated in gut tissue. Gut ISG levels positively correlated with gut HIV-1 RNA and immune activation, microbial translocation and inflammation markers. Gut IFN-I responses were not significantly different between HIV-1-infected individuals on antiretroviral treatment and uninfected controls.ConclusionThe IFN-I response is compartmentalized during chronic untreated HIV-1 infection, with IFNβ being more predominant in the gut. Gut IFN-I responses are associated with immunopathogenesis, and viral replication is likely a major driver of this response.

Published
2018

4. Low abundance of colonic butyrate-producing bacteria in HIV infection is associated with microbial translocation and immune activation

Author

Dillon, Stephanie M, Kibbie, Jon, Lee, Eric J, Guo, Kejun, Santiago, Mario L, Austin, Gregory L, Gianella, Sara, Landay, Alan L, Donovan, Andrew M, Frank, Daniel N, McCARTER, Martin D, and Wilson, Cara C

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Clinical Research, Digestive Diseases, Emerging Infectious Diseases, HIV/AIDS, 2.1 Biological and endogenous factors, Aetiology, 2.2 Factors relating to the physical environment, Infection, Inflammatory and immune system, Adult, Bacteria, Bacterial Translocation, Butyrates, Cluster Analysis, Cross-Sectional Studies, DNA, Bacterial, DNA, Ribosomal, Dysbiosis, Feces, Gastrointestinal Microbiome, HIV Infections, Humans, Intestinal Mucosa, Lymphocyte Activation, Microbiota, Phylogeny, RNA, Ribosomal, 16S, Sequence Analysis, DNA, butyrate, HIV-1 infection, microbiome, mucosal immunology, T cells, Adult Bacteria/classification/isolation & purification/*metabolism *Bacterial Translocation Butyrates/*metabolism Cluster Analysis Cross-Sectional Studies DNA, Bacterial/chemistry/genetics DNA, Ribosomal/chemistry/genetics *Dysbiosis Feces/microbiology Gastrointestinal Microbiome HIV Infections/*complications/*pathology Humans Intestinal Mucosa/microbiology/pathology/virology *Lymphocyte Activation Microbiota Phylogeny RNA, Ribosomal, 16S/genetics Sequence Analysis, DNA, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology, Biomedical and clinical sciences, Health sciences
Abstract

ObjectiveGut microbial translocation is a major driving force behind chronic immune activation during HIV-1 infection. HIV-1-related intestinal dysbiosis, including increases in mucosa-associated pathobionts, may influence microbial translocation and contribute to mucosal and systemic inflammation. Thus, it is critical to understand the mechanisms by which gut microbes and their metabolic products, such as butyrate, influence immune cell function during HIV-1 infection.DesignA cross-sectional study was performed to compare the relative abundance of butyrate-producing bacterial (BPB) species in colonic biopsies and stool of untreated, chronic HIV-1-infected (n = 18) and HIV-1-uninfected (n = 14) study participants. The effect of exogenously added butyrate on gut T-cell activation and HIV-1 infection was evaluated using an ex-vivo human intestinal cell culture model.MethodsSpecies were identified in 16S ribosomal RNA sequence datasets. Ex-vivo isolated lamina propria mononuclear cells were infected with C-C chemokine receptor type 5-tropic HIV-1Bal, cultured with enteric gram-negative bacteria and a range of butyrate doses, and lamina propria T-cell activation and HIV-1 infection levels measured.ResultsRelative abundance of total BPB and specifically of Roseburia intestinalis, were lower in colonic mucosa of HIV-1-infected versus HIV-1-uninfected individuals. In HIV-1-infected study participants, R. intestinalis relative abundance inversely correlated with systemic indicators of microbial translocation, immune activation, and vascular inflammation. Exogenous butyrate suppressed enteric gram-negative bacteria-driven lamina propria T-cell activation and HIV-1 infection levels in vitro.ConclusionReductions in mucosal butyrate from diminished colonic BPB may exacerbate pathobiont-driven gut T-cell activation and HIV replication, thereby contributing to HIV-associated mucosal pathogenesis.

Published
2017

5. Global and regional epidemiology of HIV-1 recombinants in 1990–2015: a systematic review and global survey

Author

Abimiku, Alash'le G, Agwale, Simon, Archibald, Chris, Avidor, Boaz, Barbás, María Gabriela, Barre-Sinoussi, Francoise, Barugahare, Banson, Belabbes, El Hadj, Bertagnolio, Silvia, Birx, Deborah, Bobkov, Aleksei F, Brandful, James, Bredell, Helba, Brennan, Catherine A, Brooks, James, Bruckova, Marie, Buonaguro, Luigi, Buonaguro, Franco, Buttò, Stefano, Buvé, Anne, Campbell, Mary, Carr, Jean, Carrera, Alex, Carrillo, Manuel Gómez, Celum, Connie, Chaplin, Beth, Charles, Macarthur, Chatzidimitriou, Dimitrios, Chen, Zhiwei, Chijiwa, Katsumi, Cooper, David, Cunningham, Philip, Dagnra, Anoumou, de Gascun, Cillian F, Del Amo, Julia, Delgado, Elena, Dietrich, Ursula, Dwyer, Dominic, Ellenberger, Dennis, Ensoli, Barbara, Essex, Max, Gao, Feng, Fleury, Hervé, Fonjungo, Peter N, Foulongne, Vincent, Gadkari, Deepak A, García, Federico, Garsia, Roger, Gershy-Damet, Guy Michel, Glynn, Judith R, Goodall, Ruth, Grossman, Zehava, Lindenmeyer-Guimarães, Monick, Hahn, Beatrice, Hamers, Raph L, Hamouda, Osamah, Handema, Ray, He, Xiang, Herbeck, Joshua, Ho, David D, Holguin, Africa, Hosseinipour, Mina, Hunt, Gillian, Ito, Masahiko, Bel Hadj Kacem, Mohamed Ali, Kahle, Erin, Kaleebu, Pontiano, Kalish, Marcia, Kamarulzaman, Adeeba, Kang, Chun, Kanki, Phyllis, Karamov, Edward, Karasi, Jean-Claude, Kayitenkore, Kayitesi, Kelleher, Tony, Kitayaporn, Dwip, Kostrikis, Leondios G, Kucherer, Claudia, Lara, Claudia, Leitner, Thomas, Liitsola, Kirsi, Lingappa, Jai, Linka, Marek, Lorenzana de Rivera, Ivette, Lukashov, Vladimir, Maayan, Shlomo, Mayr, Luzia, McCutchan, Francine, Meda, Nicolas, Menu, Elisabeth, Mhalu, Fred, Mloka, Doreen, Mokili, John L, Montes, Brigitte, Mor, Orna, Morgado, Mariza, Mosha, Fausta, Moussi, Awatef, Mullins, James, Najera, Rafael, Nasr, Mejda, Ndembi, Nicaise, Neilson, Joel R, Nerurkar, Vivek R, Neuhann, Florian, Nolte, Claudine, Novitsky, Vlad, Nyambi, Philippe, Ofner, Marianna, Paladin, Fem J, Papa, Anna, Pape, Jean, Parkin, Neil, Parry, Chris, Peeters, Martine, Pelletier, Alexandra, Pérez-Álvarez, Lucía, Pillay, Deenan, Pinto, Angie, Quang, Trinh Duy, Rademeyer, Cecilia, Raikanikoda, Filimone, Rayfield, Mark A, Reynes, Jean-Marc, Rinke de Wit, Tobias, Robbins, Kenneth E, Rolland, Morgane, Rousseau, Christine, Salazar-Gonzales, Jesus, Salem, Hanan, Salminen, Mika, Salomon, Horacio, Sandstrom, Paul, Santiago, Mario L, Sarr, Abdoulaye D, Schroeder, Bryan, Segondy, Michel, Selhorst, Philippe, Sempala, Sylvester, Servais, Jean, Shaik, Ansari, Shao, Yiming, Slim, Amine, Soares, Marcelo A, Songok, Elijah, Stewart, Debbie, Stokes, Julie, Subbarao, Shambavi, Sutthent, Ruengpung, Takehisa, Jun, Tanuri, Amilcar, Tee, Kok Keng, Thapa, Kiran, Thomson, Michael, Tran, Tyna, Urassa, Willy, Ushijima, Hiroshi, van de Perre, Philippe, van der Groen, Guido, van Laethem, Kristel, van Oosterhout, Joep, van Sighem, Ard, van Wijngaerden, Eric, Vandamme, Anne-Mieke, Vercauteren, Jurgen, Vidal, Nicole, Wallace, Lesley, Williamson, Carolyn, Wolday, Dawit, Xu, Jianqing, Yang, Chunfu, Zhang, Linqi, Zhang, Rong, Hemelaar, Joris, Elangovan, Ramyiadarsini, Yun, Jason, Dickson-Tetteh, Leslie, Kirtley, Shona, Gouws-Williams, Eleanor, and Ghys, Peter D

Published
2020
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6. Endogenous Retroelement Expression in the Gut Microenvironment of People Living with HIV-1

Author

Dopkins, Nicholas, primary, Fei, Tongyi, additional, Michael, Stephanie, additional, Liotta, Nicholas, additional, Guo, Kejun, additional, Mickens, Kaylee L, additional, Barrett, Brad S, additional, Bendall, Matthew L, additional, Dillon, Stephanie M, additional, Wilson, Cara C, additional, Santiago, Mario L, additional, and Nixon, Douglas F, additional

Published
2023
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8. Global and regional molecular epidemiology of HIV-1, 1990–2015: a systematic review, global survey, and trend analysis

Author

Abimiku, Alash'le G, Agwale, Simon, Archibald, Chris, Avidor, Boaz, Barbás, María Gabriela, Barre-Sinoussi, Francoise, Barugahare, Banson, Belabbes, El Hadj, Bertagnolio, Silvia, Birx, Deborah, Bobkov, Aleksei F, Brandful, James, Bredell, Helba, Brennan, Catherine A, Brooks, James, Bruckova, Marie, Buonaguro, Luigi, Buonaguro, Franco, Buttò, Stefano, Buve, Anne, Campbell, Mary, Carr, Jean, Carrera, Alex, Carrillo, Manuel Gómez, Celum, Connie, Chaplin, Beth, Charles, Macarthur, Chatzidimitriou, Dimitrios, Chen, Zhiwei, Chijiwa, Katsumi, Cooper, David, Cunningham, Philip, Dagnra, Anoumou, de Gascun, Cillian F, Del Amo, Julia, Delgado, Elena, Dietrich, Ursula, Dwyer, Dominic, Ellenberger, Dennis, Ensoli, Barbara, Essex, Max, Gao, Feng, Fleury, Herve, Fonjungo, Peter N, Foulongne, Vincent, Gadkari, Deepak A, García, Federico, Garsia, Roger, Gershy-Damet, Guy Michel, Glynn, Judith R, Goodall, Ruth, Grossman, Zehava, Lindenmeyer-Guimarães, Monick, Hahn, Beatrice, Hamers, Raph L, Hamouda, Osamah, Handema, Ray, He, Xiang, Herbeck, Joshua, Ho, David D, Holguin, Africa, Hosseinipour, Mina, Hunt, Gillian, Ito, Masahiko, Bel Hadj Kacem, Mohamed Ali, Kahle, Erin, Kaleebu, Pontiano Kaleebu, Kalish, Marcia, Kamarulzaman, Adeeba, Kang, Chun, Kanki, Phyllis, Karamov, Edward, Karasi, Jean-Claude, Kayitenkore, Kayitesi, Kelleher, Tony, Kitayaporn, Dwip, Kostrikis, Leondios G, Kucherer, Claudia, Lara, Claudia, Leitner, Thomas, Liitsola, Kirsi, Lingappa, Jai, Linka, Marek, Lorenzana de Rivera, Ivette, Lukashov, Vladimir, Maayan, Shlomo, Mayr, Luzia, McCutchan, Francine, Meda, Nicolas, Menu, Elisabeth, Mhalu, Fred, Mloka, Doreen, Mokili, John L, Montes, Brigitte, Mor, Orna, Morgado, Mariza, Mosha, Fausta, Moussi, Awatef, Mullins, James, Najera, Rafael, Nasr, Mejda, Ndembi, Nicaise, Neilson, Joel R, Nerurkar, Vivek R, Neuhann, Florian, Nolte, Claudine, Novitsky, Vlad, Nyambi, Philippe, Ofner, Marianna, Paladin, Fem J, Papa, Anna, Pape, Jean, Parkin, Neil, Parry, Chris, Peeters, Martine, Pelletier, Alexandra, Pérez-Álvarez, Lucía, Pillay, Deenan, Pinto, Angie, Quang, Trinh Duy, Rademeyer, Cecilia, Raikanikoda, Filimone, Rayfield, Mark A, Reynes, Jean-Marc, Rinke de Wit, Tobias, Robbins, Kenneth E, Rolland, Morgane, Rousseau, Christine, Salazar-Gonzales, Jesus, Salem, Hanan, Salminen, Mika, Salomon, Horacio, Sandstrom, Paul, Santiago, Mario L, Sarr, Abdoulaye D, Schroeder, Bryan, Segondy, Michel, Selhorst, Philippe, Sempala, Sylvester, Servais, Jean, Shaik, Ansari, Shao, Yiming, Slim, Amine, Soares, Marcelo A, Songok, Elijah, Stewart, Debbie, Stokes, Julie, Subbarao, Shambavi, Sutthent, Ruengpung, Takehisa, Jun, Tanuri, Amilcar, Tee, Kok Keng, Thapa, Kiran, Thomson, Michael, Tran, Tyna, Urassa, Willy, Ushijima, Hiroshi, van de Perre, Philippe, van der Groen, Guido, van Laethem, Kristel, van Oosterhout, Joep, van Sighem, Ard, van Wijngaerden, Eric, Vandamme, Anne-Mieke, Vercauteren, Jurgen, Vidal, Nicole, Wallace, Lesley, Williamson, Carolyn, Wolday, Dawit, Xu, Jianqing, Yang, Chunfu, Zhang, Linqi, Zhang, Rong, Hemelaar, Joris, Elangovan, Ramyiadarsini, Yun, Jason, Dickson-Tetteh, Leslie, Fleminger, Isabella, Kirtley, Shona, Williams, Brian, Gouws-Williams, Eleanor, and Ghys, Peter D

Published
2019
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9. Enhanced Fusion and Virion Incorporation for HIV-1 Subtype C Envelope Glycoproteins with Compact V1/V2 Domains

Author

Cavrois, Marielle, Neidleman, Jason, Santiago, Mario L, Derdeyn, Cynthia A, Hunter, Eric, and Greene, Warner C

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, HIV/AIDS, Immunization, Vaccine Related, Sexually Transmitted Infections, Prevention, Infection, Good Health and Well Being, Base Sequence, Cloning, Molecular, DNA Primers, Enzyme-Linked Immunosorbent Assay, Genetic Engineering, Genetic Variation, HIV-1, Humans, Molecular Sequence Data, Protein Structure, Tertiary, Sequence Alignment, Sequence Analysis, DNA, Virus Integration, env Gene Products, Human Immunodeficiency Virus, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract

In infected people, the HIV-1 envelope glycoprotein (Env) constantly evolves to escape the immune response while retaining the essential elements needed to mediate viral entry into target cells. The extensive genetic variation of Env is particularly striking in the V1/V2 hypervariable domains. In this study, we investigated the trade-off, in terms of fusion efficiency, for encoding V1/V2 domains of different lengths. We found that natural variations in V1/V2 length exert a profound impact on HIV-1 entry. Variants encoding compact V1/V2 domains mediated fusion with higher efficiencies than related Envs encoding longer V1/V2 domains. By exchanging the V1/V2 domains between Envs of the same infected person or between two persons linked by a transmission event, we further demonstrated that V1/V2 domains critically influence both Env incorporation into viral particles and fusion to primary CD4 T cells and monocyte-derived dendritic cells. Shortening the V1/V2 domains consistently increased Env incorporation and fusion, whereas lengthening the V1/V2 domains decreased Env incorporation and fusion. Given that in a new host transmitted founder viruses are distinguished by compact Envs with fewer glycosylation sites, our study points to fusion and possibly Env incorporation into virions as limiting steps for transmission of HIV-1 to a new host and suggests that the length and/or the N-glycosylation profile of the V1/V2 domain influences these early steps in the HIV life cycle.

Published
2014

10. Regulation of interferon signaling by transposon exonization

Author

Pasquesi, Giulia Irene Maria, primary, Allen, Holly, additional, Ivancevic, Atma, additional, Barbachano-Guerrero, Arturo, additional, Joyner, Olivia, additional, Guo, Kejun, additional, Simpson, David M, additional, Gapin, Keala, additional, Horton, Isabella, additional, Nguyen, Lily, additional, Yang, Qing, additional, Warren, Cody J, additional, Florea, Liliana D, additional, Bitler, Benjamin G, additional, Santiago, Mario L, additional, Sawyer, Sara L, additional, and Chuong, Edward B, additional

Published
2023
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12. 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

13. Noninfectious retrovirus particles drive the APOBEC3/Rfv3 dependent neutralizing antibody response.

Author

Smith, Diana S, Guo, Kejun, Barrett, Bradley S, Heilman, Karl J, Evans, Leonard H, Hasenkrug, Kim J, Greene, Warner C, and Santiago, Mario L

Subjects
Plasma, Animals, Mice, Inbred BALB C, Mice, Knockout, Mice, Friend murine leukemia virus, Virion, Cytidine Deaminase, RNA, Viral, Antiviral Agents, Viral Load, Sequence Analysis, RNA, Antibody Formation, Reverse Transcription, Phenotype, Promoter Regions, Genetic, Antibodies, Neutralizing, Inbred BALB C, Knockout, RNA, Viral, Sequence Analysis, Promoter Regions, Genetic, Antibodies, Neutralizing, Virology, Microbiology, Immunology, Medical Microbiology
Abstract

Members of the APOBEC3 family of deoxycytidine deaminases counteract a broad range of retroviruses in vitro through an indirect mechanism that requires virion incorporation and inhibition of reverse transcription and/or hypermutation of minus strand transcripts in the next target cell. The selective advantage to the host of this indirect restriction mechanism remains unclear, but valuable insights may be gained by studying APOBEC3 function in vivo. Apobec3 was previously shown to encode Rfv3, a classical resistance gene that controls the recovery of mice from pathogenic Friend retrovirus (FV) infection by promoting a more potent neutralizing antibody (NAb) response. The underlying mechanism does not involve a direct effect of Apobec3 on B cell function. Here we show that while Apobec3 decreased titers of infectious virus during acute FV infection, plasma viral RNA loads were maintained, indicating substantial release of noninfectious particles in vivo. The lack of plasma virion infectivity was associated with a significant post-entry block during early reverse transcription rather than G-to-A hypermutation. The Apobec3-dependent NAb response correlated with IgG binding titers against native, but not detergent-lysed virions. These findings indicate that innate Apobec3 restriction promotes NAb responses by maintaining high concentrations of virions with native B cell epitopes, but in the context of low virion infectivity. Finally, Apobec3 restriction was found to be saturable in vivo, since increasing FV inoculum doses resulted in decreased Apobec3 inhibition. By analogy, maximizing the release of noninfectious particles by modulating APOBEC3 expression may improve humoral immunity against pathogenic human retroviral infections.

Published
2011

14. Immunotherapy-induced cytotoxic T follicular helper cells reduce numbers of retrovirus-infected reservoir cells in B cell follicles.

Author

Malyshkina, Anna, Bayer, Wibke, Podschwadt, Philip, Otto, Lucas, Karakoese, Zehra, Sutter, Kathrin, Bruderek, Kirsten, Wang, Baoxiao, Lavender, Kerry J., Santiago, Mario L., Leipe, Pia Madeleine, Elsner, Carina, Esser, Stefan, Brandau, Sven, Gunzer, Matthias, and Dittmer, Ulf

Subjects
B cells, T helper cells, CYTOTOXIC T cells, ANTIBODY formation, LYMPH nodes, GERMINAL centers, TERMINATION of treatment, OVARIAN follicle
Abstract

Antiretroviral therapy (ART) transformed HIV from a life-threatening disease to a chronic condition. However, eliminating the virus remains an elusive therapy goal. For several decades, Friend virus (FV) infection serves as a murine model to study retrovirus immunity. Similar to HIV, FV persists at low levels in lymph nodes B cell follicles avoiding elimination by immune cells. Such immune-privileged reservoirs exclude cytotoxic T cells from entry. However, CXCR5+ T cells are permitted to traffic through germinal centers. This marker is predominantly expressed by CD4+ follicular helper T cells (Tfh). Therefore, we explored immunotherapy to induce cytotoxic Tfh, which are rarely found under physiological conditions. The TNF receptor family member CD137 was first identified as a promising target for cancer immunotherapy. We demonstrated that FV-infected mice treatment with αCD137 antibody resulted in an induction of the cytotoxic program in Tfh. The therapy significantly increased numbers of cytotoxic Tfh within B cell follicles and contributed to viral load reduction. Moreover, αCD137 antibody combined with ART delayed virus rebound upon treatment termination without disturbing the lymph node architecture or antibody responses. Thus, αCD137 antibody therapy might be a novel strategy to target the retroviral reservoir and an interesting approach for HIV cure research. Author summary: Despite the development of potent antiretroviral therapy, elimination of the HIV reservoir from lymph nodes remains elusive. The main reason is that lymph nodes are an immune privileged site in which cytotoxic T cell activity is restricted. We used the Friend retrovirus (FV) mouse model to develop a novel therapy approach that targets the retroviral reservoir in lymph nodes. Immunotherapy with CD137 activating antibodies induced a cytotoxic program in follicular CD4+ T cells, which improved their killing capacity and resulted in a reduction of the FV reservoir in lymph nodes. Antibody treatment combined with antiretroviral therapy delayed virus rebound upon treatment termination without disturbing the lymph node architecture or antibody responses to unrelated antigens. Thus, αCD137 antibody therapy might be a novel strategy to target the retroviral reservoir in lymph nodes and an interesting approach for HIV cure research. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Clinical and Economic Impact of COVID-19 on Agricultural Workers, Guatemala1

Author

Olson, Daniel, primary, Calvimontes, Diva M., additional, Lamb, Molly M., additional, Guzman, Gerber, additional, Barrios, Edgar, additional, Chacon, Andrea, additional, Rojop, Neudy, additional, Arias, Kareen, additional, Gomez, Melissa, additional, Bolanos, Guillermo A., additional, Monzon, Jose, additional, Chard, Anna N., additional, Iwamoto, Chelsea, additional, Duca, Lindsey M., additional, Vuong, Nga, additional, Fineman, Melissa, additional, Lesteberg, Kelsey, additional, Beckham, David, additional, Santiago, Mario L., additional, Quicke, Kendra, additional, Ebel, Gregory, additional, Gutierrez, Emily Zielinski, additional, Azziz-Baumgartner, Eduardo, additional, Hayden, Frederick G., additional, Mansour, Hani, additional, Edwards, Kathryn, additional, Newman, Lee S., additional, and Asturias, Edwin J., additional

Published
2023
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17. Altered Immunoglobulin Repertoire and Decreased IgA Somatic Hypermutation in the Gut during Chronic HIV-1 Infection

Author

Jones, Sean T., primary, Guo, Kejun, additional, Cooper, Emily H., additional, Dillon, Stephanie M., additional, Wood, Cheyret, additional, Nguyen, David H., additional, Shen, Guannan, additional, Barrett, Bradley S., additional, Frank, Daniel N., additional, Kroehl, Miranda, additional, Janoff, Edward N., additional, Kechris, Katerina, additional, Wilson, Cara C., additional, and Santiago, Mario L., additional

Published
2022
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18. Interferon resistance of emerging SARS-CoV-2 variants

Author

Guo, Kejun, primary, Barrett, Bradley S., additional, Morrison, James H., additional, Mickens, Kaylee L., additional, Vladar, Eszter K., additional, Hasenkrug, Kim J., additional, Poeschla, Eric M., additional, and Santiago, Mario L., additional

Published
2022
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19. High SARS-CoV-2 Seroprevalence and Rapid Neutralizing Antibody Decline among Agricultural Workers in Rural Guatemala, June 2020–March 2021

Author

Iwamoto, Chelsea, primary, Lesteberg, Kelsey E., additional, Lamb, Molly M., additional, Calvimontes, Diva M., additional, Guo, Kejun, additional, Barrett, Bradley S., additional, Mickens, Kaylee L., additional, Duca, Lindsey M., additional, Monzon, Jose, additional, Chard, Anna N., additional, Guzman, Gerber, additional, Barrios, Edgar, additional, Rojop, Neudy, additional, Arias, Kareen, additional, Gomez, Melissa, additional, Paiz, Claudia, additional, Bolanos, Guillermo Antonio, additional, Edwards, Kathryn M., additional, Zielinski Gutierrez, Emily, additional, Azziz-Baumgartner, Eduardo, additional, Asturias, Edwin J., additional, Santiago, Mario L., additional, Beckham, J. David, additional, and Olson, Daniel, additional

Published
2022
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23. Granzyme B+ CD4 T cells accumulate in the colon during chronic HIV-1 infection

Author

Dillon, Stephanie M., primary, Mickens, Kaylee L., additional, Thompson, Tezha A., additional, Cooper, Emily H., additional, Nesladek, Sabrina, additional, Christians, Allison J., additional, Castleman, Moriah, additional, Guo, Kejun, additional, Wood, Cheyret, additional, Frank, Daniel N., additional, Kechris, Katerina, additional, Santiago, Mario L., additional, and Wilson, Cara C., additional

Published
2022
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24. Specialized interferon action in COVID-19

Author

Galbraith, Matthew D., primary, Kinning, Kohl T., additional, Sullivan, Kelly D., additional, Araya, Paula, additional, Smith, Keith P., additional, Granrath, Ross E., additional, Shaw, Jessica R., additional, Baxter, Ryan, additional, Jordan, Kimberly R., additional, Russell, Seth, additional, Dzieciatkowska, Monika, additional, Reisz, Julie A., additional, Gamboni, Fabia, additional, Cendali, Francesca, additional, Ghosh, Tusharkanti, additional, Guo, Kejun, additional, Wilson, Cara C., additional, Santiago, Mario L., additional, Monte, Andrew A., additional, Bennett, Tellen D., additional, Hansen, Kirk C., additional, Hsieh, Elena W. Y., additional, D’Alessandro, Angelo, additional, and Espinosa, Joaquin M., additional

Published
2022
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25. Clinical and Economic Impact of COVID-19 on Plantation Workers: Preliminary Results from the Guatemala Agricultural Workers and Respiratory Illness Impact (AGRI) Study

Author

Olson, Daniel, primary, Calvimontes, Diva M., additional, Lamb, Molly M., additional, Guzman, Gerber, additional, Barrios, Edgar, additional, Chacon, Andrea, additional, Rojop, Neudy, additional, Arias, Kareen, additional, Gomez, Melissa, additional, Bolanos, Guillermo Antonio, additional, Monzon, Jose, additional, Chard, Anna N., additional, Iwamoto, Chelsea, additional, Duca, Lindsey M., additional, Vuong, Nga, additional, Fineman, Melissa, additional, Lesteberg, Kelsey, additional, Beckham, David, additional, Santiago, Mario L., additional, Quicke, Kendra, additional, Ebel, Gregory, additional, Gutierrez, Emily Zielinski, additional, Azziz-Baumgartner, Eduardo, additional, Hayden, Frederick G., additional, Mansour, Hani, additional, Edwards, Kathryn, additional, Newman, Lee S., additional, and Asturias, Edwin J., additional

Published
2022
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26. SAMHD1 Promotes the Antiretroviral Adaptive Immune Response in Mice Exposed to Lipopolysaccharide

Author

Barrett, BradleyS., primary, Nguyen, David H., additional, Xu, Joella, additional, Guo, Kejun, additional, Shetty, Shravida, additional, Jones, Sean T., additional, Mickens, Kaylee L., additional, Shepard, Caitlin, additional, Roers, Axel, additional, Behrendt, Rayk, additional, Wu, Li, additional, Kim, Baek, additional, and Santiago, Mario L., additional

Published
2022
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27. COVID-19 Serology Control Panel Using the Dried-Tube Specimen Method

Author

Windsor, William J., primary, Knight, Vijaya, additional, Merkel, Patricia A., additional, Lamb, Molly M., additional, Tucker, Heidi R., additional, Carson, Kyle, additional, Howard, Kelly M., additional, Yates, Jennifer L., additional, Santiago, Mario L., additional, McCarthy, Mary K., additional, Morrison, Thomas E., additional, Kedl, Ross M., additional, Frazer-Abel, Ashley, additional, Guo, Kejun, additional, Andersen, Gillian, additional, Huey, Leah, additional, Barrett, Bradley S., additional, Colón-Franco, Jessica M., additional, Lee, William T., additional, and Chu, May C., additional

Published
2022
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31. Recovery from Acute SARS-CoV-2 Infection and Development of Anamnestic Immune Responses in T Cell-Depleted Rhesus Macaques

Author

Hasenkrug, Kim J., primary, Feldmann, Friederike, additional, Myers, Lara, additional, Santiago, Mario L., additional, Guo, Kejun, additional, Barrett, Bradley S., additional, Mickens, Kaylee L., additional, Carmody, Aaron, additional, Okumura, Atsushi, additional, Rao, Deepashri, additional, Collins, Madison M., additional, Messer, Ronald J., additional, Lovaglio, Jamie, additional, Shaia, Carl, additional, Rosenke, Rebecca, additional, van Doremalen, Neeltje, additional, Clancy, Chad, additional, Saturday, Greg, additional, Hanley, Patrick, additional, Smith, Brian J., additional, Meade-White, Kimberly, additional, Shupert, W. Lesley, additional, Hawman, David W., additional, and Feldmann, Heinz, additional

Published
2021
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32. COVID-19 Serology Control Panel Using the Dried Tube Specimen Method

Author

Windsor, William J., primary, Knight, Vijaya, additional, Merkel, Patricia A., additional, Lamb, Molly M., additional, Santiago, Mario L., additional, McCarthy, Mary K., additional, Morrison, Thomas E., additional, Kedl, Ross M., additional, Frazer-Abel, Ashley, additional, Guo, Kejun, additional, Andersen, Gillian, additional, Huey, Leah, additional, Barrett, Bradley S., additional, Colón-Franco, Jessica M., additional, and Chu, May C., additional

Published
2021
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34. Interferon resistance of emerging SARS-CoV-2 variants.

Author

Kejun Guo, Barrett, Bradley S., Morrison, James H., Mickens, Kaylee L., Vladar, Eszter K., Hasenkrug, Kim J., Poeschla, Eric M., and Santiago, Mario L.

Subjects
SARS-CoV-2, INTERFERONS, SARS-CoV-2 Delta variant, SARS-CoV-2 Omicron variant, VIRAL genes, GENETIC counseling
Abstract

The emergence of SARS-CoV-2 variants with enhanced transmissibility, pathogenesis, and resistance to vaccines presents urgent challenges for curbing the COVID-19 pandemic. While Spike mutations that enhance virus infectivity or neutralizing antibody evasion may drive the emergence of these novel variants, studies documenting a critical role for interferon responses in the early control of SARS-CoV-2 infection, combined with the presence of viral genes that limit these responses, suggest that interferons may also influence SARS-CoV-2 evolution. Here, we compared the potency of 17 different human interferons against multiple viral lineages sampled during the course of the global outbreak, including ancestral and five major variants of concern that include the B.1.1.7 (alpha), B.1.351 (beta), P.1 (gamma), B.1.617.2 (delta), and B.1.1.529 (omicron) lineages. Our data reveal that relative to ancestral isolates, SARS-CoV-2 variants of concern exhibited increased interferon resistance, suggesting that evasion of innate immunity may be a significant, ongoing driving force for SARS-CoV-2 evolution. These findings have implications for the increased transmissibility and/or lethality of emerging variants and highlight the interferon subtypes that may be most successful in the treatment of early infections. [ABSTRACT FROM AUTHOR]

Published
2022
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37. Interferon Resistance of Emerging SARS-CoV-2 Variants

Author

Guo, Kejun, primary, Barrett, Bradley S., additional, Mickens, Kaylee L., additional, Vladar, Ezster K., additional, Morrison, James H., additional, Hasenkrug, Kim J., additional, Poeschla, Eric M., additional, and Santiago, Mario L., additional

Published
2021
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38. HIV infection does not alter interferon α/β receptor 2 expression on mucosal immune cells

Author

Ickler, Julia, Francois, Sandra, Widera, Marek, Santiago, Mario L., Dittmer, Ulf, and Sutter, Kathrin

Subjects
RNA viruses, B Cells, Medizin, HIV Infections, Receptor, Interferon alpha-beta, Pathology and Laboratory Medicine, Biochemistry, White Blood Cells, Immunodeficiency Viruses, Animal Cells, Medicine and Health Sciences, T Cells, Messenger RNA, virus diseases, Medizinische Fakultät » Universitätsklinikum Essen » Institut für Virologie, Nucleic acids, Medical Microbiology, Viral Pathogens, Viruses, Interferon Type I, Medicine, Infectious diseases, Cellular Types, Pathogens, Research Article, Signal Transduction, Lymphoid Tissue, Science, Immune Cells, Immunology, Cytotoxic T cells, Viral diseases, Microbiology, Antiviral Agents, Retroviruses, Humans, ddc:610, Antibody-Producing Cells, Microbial Pathogens, Immunity, Mucosal, Blood Cells, Lentivirus, Organisms, Biology and Life Sciences, Proteins, HIV, Cell Biology, Immunity, Innate, RNA, Interferons
Abstract

The innate immune response induced by type I interferons (IFNs) plays a critical role in the establishment of HIV infection. IFNs are induced early in HIV infection and trigger an antiviral defense program by signaling through the IFNα/β receptor (IFNAR), which consists of two subunits, IFNAR1 and IFNAR2. Changes in IFNAR expression in HIV target cells, as well as other immune cells, could therefore have important consequences for initial HIV spread. It was previously reported that IFNAR2 expression is increased in peripheral blood CD4+ CXCR4+ T cells of HIV+ patients compared to HIV uninfected controls, suggesting that HIV infection may alter the IFN responsiveness of target cells. However, the earliest immune cells affected by HIV in vivo reside in the gut-associated lymphoid tissue (GALT). To date, it remains unknown if IFNAR expression is altered in GALT immune cells in the context of HIV infection and exposure to IFNs, including the 12 IFNα subtypes. Here, we analyzed the expression of surface bound and soluble IFNAR2 on Lamina propria mononuclear cells (LPMCs) isolated from the GALT of HIV- individuals and in plasma samples of HIV+ patients. IFNAR2 expression varied between different T cells, B cells and natural killer cells, but was not altered following HIV infection. Furthermore, expression of the soluble IFNAR2a isoform was not changed in HIV+ patients compared to healthy donors, nor in LPMCs after HIV-1 infection ex vivo. Even though the 12 human IFNα subtypes trigger different biological responses and vary in their affinity to both receptor subunits, stimulation of LPMCs with different recombinant IFNα subtypes did not result in any significant changes in IFNAR2 surface expression. Our data suggests that potential changes in the IFN responsiveness of mucosal immune cells during HIV infection are unlikely dictated by changes in IFNAR2 expression. OA Förderung 2020

Published
2020

39. Global and regional epidemiology of HIV-1 recombinants in 1990–2015: a systematic review and global survey

Author

Hemelaar, Joris, primary, Elangovan, Ramyiadarsini, additional, Yun, Jason, additional, Dickson-Tetteh, Leslie, additional, Kirtley, Shona, additional, Gouws-Williams, Eleanor, additional, Ghys, Peter D, additional, Abimiku, Alash'le G, additional, Agwale, Simon, additional, Archibald, Chris, additional, Avidor, Boaz, additional, Barbás, María Gabriela, additional, Barre-Sinoussi, Francoise, additional, Barugahare, Banson, additional, Belabbes, El Hadj, additional, Bertagnolio, Silvia, additional, Birx, Deborah, additional, Bobkov, Aleksei F, additional, Brandful, James, additional, Bredell, Helba, additional, Brennan, Catherine A, additional, Brooks, James, additional, Bruckova, Marie, additional, Buonaguro, Luigi, additional, Buonaguro, Franco, additional, Buttò, Stefano, additional, Buvé, Anne, additional, Campbell, Mary, additional, Carr, Jean, additional, Carrera, Alex, additional, Carrillo, Manuel Gómez, additional, Celum, Connie, additional, Chaplin, Beth, additional, Charles, Macarthur, additional, Chatzidimitriou, Dimitrios, additional, Chen, Zhiwei, additional, Chijiwa, Katsumi, additional, Cooper, David, additional, Cunningham, Philip, additional, Dagnra, Anoumou, additional, de Gascun, Cillian F, additional, Del Amo, Julia, additional, Delgado, Elena, additional, Dietrich, Ursula, additional, Dwyer, Dominic, additional, Ellenberger, Dennis, additional, Ensoli, Barbara, additional, Essex, Max, additional, Gao, Feng, additional, Fleury, Hervé, additional, Fonjungo, Peter N, additional, Foulongne, Vincent, additional, Gadkari, Deepak A, additional, García, Federico, additional, Garsia, Roger, additional, Gershy-Damet, Guy Michel, additional, Glynn, Judith R, additional, Goodall, Ruth, additional, Grossman, Zehava, additional, Lindenmeyer-Guimarães, Monick, additional, Hahn, Beatrice, additional, Hamers, Raph L, additional, Hamouda, Osamah, additional, Handema, Ray, additional, He, Xiang, additional, Herbeck, Joshua, additional, Ho, David D, additional, Holguin, Africa, additional, Hosseinipour, Mina, additional, Hunt, Gillian, additional, Ito, Masahiko, additional, Bel Hadj Kacem, Mohamed Ali, additional, Kahle, Erin, additional, Kaleebu, Pontiano, additional, Kalish, Marcia, additional, Kamarulzaman, Adeeba, additional, Kang, Chun, additional, Kanki, Phyllis, additional, Karamov, Edward, additional, Karasi, Jean-Claude, additional, Kayitenkore, Kayitesi, additional, Kelleher, Tony, additional, Kitayaporn, Dwip, additional, Kostrikis, Leondios G, additional, Kucherer, Claudia, additional, Lara, Claudia, additional, Leitner, Thomas, additional, Liitsola, Kirsi, additional, Lingappa, Jai, additional, Linka, Marek, additional, Lorenzana de Rivera, Ivette, additional, Lukashov, Vladimir, additional, Maayan, Shlomo, additional, Mayr, Luzia, additional, McCutchan, Francine, additional, Meda, Nicolas, additional, Menu, Elisabeth, additional, Mhalu, Fred, additional, Mloka, Doreen, additional, Mokili, John L, additional, Montes, Brigitte, additional, Mor, Orna, additional, Morgado, Mariza, additional, Mosha, Fausta, additional, Moussi, Awatef, additional, Mullins, James, additional, Najera, Rafael, additional, Nasr, Mejda, additional, Ndembi, Nicaise, additional, Neilson, Joel R, additional, Nerurkar, Vivek R, additional, Neuhann, Florian, additional, Nolte, Claudine, additional, Novitsky, Vlad, additional, Nyambi, Philippe, additional, Ofner, Marianna, additional, Paladin, Fem J, additional, Papa, Anna, additional, Pape, Jean, additional, Parkin, Neil, additional, Parry, Chris, additional, Peeters, Martine, additional, Pelletier, Alexandra, additional, Pérez-Álvarez, Lucía, additional, Pillay, Deenan, additional, Pinto, Angie, additional, Quang, Trinh Duy, additional, Rademeyer, Cecilia, additional, Raikanikoda, Filimone, additional, Rayfield, Mark A, additional, Reynes, Jean-Marc, additional, Rinke de Wit, Tobias, additional, Robbins, Kenneth E, additional, Rolland, Morgane, additional, Rousseau, Christine, additional, Salazar-Gonzales, Jesus, additional, Salem, Hanan, additional, Salminen, Mika, additional, Salomon, Horacio, additional, Sandstrom, Paul, additional, Santiago, Mario L, additional, Sarr, Abdoulaye D, additional, Schroeder, Bryan, additional, Segondy, Michel, additional, Selhorst, Philippe, additional, Sempala, Sylvester, additional, Servais, Jean, additional, Shaik, Ansari, additional, Shao, Yiming, additional, Slim, Amine, additional, Soares, Marcelo A, additional, Songok, Elijah, additional, Stewart, Debbie, additional, Stokes, Julie, additional, Subbarao, Shambavi, additional, Sutthent, Ruengpung, additional, Takehisa, Jun, additional, Tanuri, Amilcar, additional, Tee, Kok Keng, additional, Thapa, Kiran, additional, Thomson, Michael, additional, Tran, Tyna, additional, Urassa, Willy, additional, Ushijima, Hiroshi, additional, van de Perre, Philippe, additional, van der Groen, Guido, additional, van Laethem, Kristel, additional, van Oosterhout, Joep, additional, van Sighem, Ard, additional, van Wijngaerden, Eric, additional, Vandamme, Anne-Mieke, additional, Vercauteren, Jurgen, additional, Vidal, Nicole, additional, Wallace, Lesley, additional, Williamson, Carolyn, additional, Wolday, Dawit, additional, Xu, Jianqing, additional, Yang, Chunfu, additional, Zhang, Linqi, additional, and Zhang, Rong, additional

Published
2020
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40. Qualitative Differences Between the IFNα subtypes and IFNβ Influence Chronic Mucosal HIV-1 Pathogenesis

Author

Guo, Kejun, primary, Shen, Guannan, additional, Kibbie, Jon, additional, Gonzalez, Tania, additional, Dillon, Stephanie M., additional, Smith, Harry A., additional, Cooper, Emily H., additional, Lavender, Kerry, additional, Hasenkrug, Kim J., additional, Sutter, Kathrin, additional, Dittmer, Ulf, additional, Kroehl, Miranda, additional, Kechris, Katerina, additional, Wilson, Cara C., additional, and Santiago, Mario L., additional

Published
2020
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43. Nef-mediated TCR-CD3 and MHC-I down-modulation prevents CD4+ T cell depletion in natural SIV infection

Author

Sharp Paul, Sodora Donald L, Roques Pierre, Bailes Elizabeth, Courgnaud Valerie, Peeters Martine, Novembre Francis J, Müller-Trutwin Michaela C, Bibollet-Ruche Frederic, Santiago Mario L, Li Hui, Kutsch Olaf, Münch Jan, Schindler Michael, Silvestri Guido, Hahn Beatrice H, and Kirchhoff Frank

Subjects
Immunologic diseases. Allergy, RC581-607
Published
2006
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44. Contributors

Author

Andino, Raul, primary, Arnold, Jamie J., additional, Barrett, John W., additional, Bernard, Hans-Ulrich, additional, Biebricher, Christof K., additional, Bonhoeffer, Sebastian, additional, Bosch, A., additional, Bull, J.J., additional, Buti, M., additional, Cameron, Craig E., additional, Daròs, José-Antonio, additional, Davison, Andrew J., additional, Dolan, Aidan, additional, Domingo, Esteban, additional, Duran-Vila, Núria, additional, Elena, Santiago F., additional, Escarmís, Cristina, additional, Esteban, J.I., additional, Flores, Richard, additional, García-Arenal, Fernando, additional, Gatherer, Derek, additional, Gibbs, Adrian, additional, Gibbs, Mark, additional, Greene, Warner C., additional, Hanley, Kathryn A., additional, Hendrix, Roger W., additional, Herrera, Mónica, additional, Hoelzer, Karin, additional, Holland, John J., additional, Holmes, Edward C., additional, Jardí, R., additional, Martell, M., additional, McFadden, Grant, additional, McGeoch, Duncan J., additional, Menéndez-Arias, Luis, additional, Müller, Viktor, additional, Novella, Isabel S., additional, Ohshima, Kazusato, additional, Parrish, Colin R., additional, Perales, Celia, additional, Quer, J., additional, Rodriguez, F., additional, Roossinck, Marilyn J., additional, Sannjuán, R., additional, Santiago, Mario L., additional, Schuster, Peter, additional, Sevilla-Reyes, Edgar E., additional, Smidansky, Eric, additional, Stadler, Peter F., additional, Van Rij, Ronald, additional, Villareal, Luis P., additional, Wain-Hobson, Simon, additional, Weaver, Scott C., additional, and Wilke, C.O., additional

Published
2008
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48. Global and regional molecular epidemiology of HIV-1, 1990–2015: a systematic review, global survey, and trend analysis

Author

Hemelaar, Joris, Elangovan, Ramyiadarsini, Yun, Jason, Dickson-Tetteh, Leslie, Fleminger, Isabella, Kirtley, Shona, Williams, Brian, Gouws-Williams, Eleanor, Ghys, Peter D, Abimiku, Alash'le G, Agwale, Simon, Archibald, Chris, Avidor, Boaz, Barbás, María Gabriela, Barre-Sinoussi, Francoise, Barugahare, Banson, Belabbes, El Hadj, Bertagnolio, Silvia, Birx, Deborah, Bobkov, Aleksei F, Brandful, James, Bredell, Helba, Brennan, Catherine A, Brooks, James, Bruckova, Marie, Buonaguro, Luigi, Buonaguro, Franco, Buttò, Stefano, Buve, Anne, Campbell, Mary, Carr, Jean, Carrera, Alex, Carrillo, Manuel Gómez, Celum, Connie, Chaplin, Beth, Charles, Macarthur, Chatzidimitriou, Dimitrios, Chen, Zhiwei, Chijiwa, Katsumi, Cooper, David, Cunningham, Philip, Dagnra, Anoumou, de Gascun, Cillian F, Del Amo, Julia, Delgado, Elena, Dietrich, Ursula, Dwyer, Dominic, Ellenberger, Dennis, Ensoli, Barbara, Essex, Max, Gao, Feng, Fleury, Herve, Fonjungo, Peter N, Foulongne, Vincent, Gadkari, Deepak A, García, Federico, Garsia, Roger, Gershy-Damet, Guy Michel, Glynn, Judith R, Goodall, Ruth, Grossman, Zehava, Lindenmeyer-Guimarães, Monick, Hahn, Beatrice, Hamers, Raph L, Hamouda, Osamah, Handema, Ray, He, Xiang, Herbeck, Joshua, Ho, David D, Holguin, Africa, Hosseinipour, Mina, Hunt, Gillian, Ito, Masahiko, Bel Hadj Kacem, Mohamed Ali, Kahle, Erin, Kaleebu, Pontiano Kaleebu, Kalish, Marcia, Kamarulzaman, Adeeba, Kang, Chun, Kanki, Phyllis, Karamov, Edward, Karasi, Jean-Claude, Kayitenkore, Kayitesi, Kelleher, Tony, Kitayaporn, Dwip, Kostrikis, Leondios G, Kucherer, Claudia, Lara, Claudia, Leitner, Thomas, Liitsola, Kirsi, Lingappa, Jai, Linka, Marek, Lorenzana de Rivera, Ivette, Lukashov, Vladimir, Maayan, Shlomo, Mayr, Luzia, McCutchan, Francine, Meda, Nicolas, Menu, Elisabeth, Mhalu, Fred, Mloka, Doreen, Mokili, John L, Montes, Brigitte, Mor, Orna, Morgado, Mariza, Mosha, Fausta, Moussi, Awatef, Mullins, James, Najera, Rafael, Nasr, Mejda, Ndembi, Nicaise, Neilson, Joel R, Nerurkar, Vivek R, Neuhann, Florian, Nolte, Claudine, Novitsky, Vlad, Nyambi, Philippe, Ofner, Marianna, Paladin, Fem J, Papa, Anna, Pape, Jean, Parkin, Neil, Parry, Chris, Peeters, Martine, Pelletier, Alexandra, Pérez-Álvarez, Lucía, Pillay, Deenan, Pinto, Angie, Quang, Trinh Duy, Rademeyer, Cecilia, Raikanikoda, Filimone, Rayfield, Mark A, Reynes, Jean-Marc, Rinke de Wit, Tobias, Robbins, Kenneth E, Rolland, Morgane, Rousseau, Christine, Salazar-Gonzales, Jesus, Salem, Hanan, Salminen, Mika, Salomon, Horacio, Sandstrom, Paul, Santiago, Mario L, Sarr, Abdoulaye D, Schroeder, Bryan, Segondy, Michel, Selhorst, Philippe, Sempala, Sylvester, Servais, Jean, Shaik, Ansari, Shao, Yiming, Slim, Amine, Soares, Marcelo A, Songok, Elijah, Stewart, Debbie, Stokes, Julie, Subbarao, Shambavi, Sutthent, Ruengpung, Takehisa, Jun, Tanuri, Amilcar, Tee, Kok Keng, Thapa, Kiran, Thomson, Michael, Tran, Tyna, Urassa, Willy, Ushijima, Hiroshi, van de Perre, Philippe, van der Groen, Guido, van Laethem, Kristel, van Oosterhout, Joep, van Sighem, Ard, van Wijngaerden, Eric, Vandamme, Anne-Mieke, Vercauteren, Jurgen, Vidal, Nicole, Wallace, Lesley, Williamson, Carolyn, Wolday, Dawit, Xu, Jianqing, Yang, Chunfu, Zhang, Linqi, Zhang, Rong, John Radcliffe Hospital [Oxford University Hospital], Centre for Statistics in Medicine, University of Oxford [Oxford], Stellenbosch University, UNAIDS [Genève, Suisse] (ONUSIDA), Institut Pasteur [Paris], Noguchi Memorial Institute for Medical Research [Accra, Ghana] (NMIMR), University of Ghana, Institute of Tropical Medicine [Antwerp] (ITM), State Key Laboratory of Silkworm Genome Biology, Southwest University, Commissariat à l'énergie atomique et aux énergies alternatives - Laboratoire d'Electronique et de Technologie de l'Information (CEA-LETI), Direction de Recherche Technologique (CEA) (DRT (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Georg-Speyer-Haus, The University of Sydney, National AIDS Centre, Istituto Superiore di Sanita [Rome], Harvard School of Public Health, Digital Enterprise Research Institute (DERI-NUIG), National University of Ireland [Galway] (NUI Galway), Microbiologie cellulaire et moléculaire et pathogénicité (MCMP), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Virologie, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Pathogénèse et contrôle des infections chroniques (PCCI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre Hospitalier Universitaire de Montpellier (CHU Montpellier ), Departments of Medicine and Microbiology, University of Alabama at Birmingham [ Birmingham] (UAB), Robert Koch Institute [Berlin] (RKI), Beihang University (BUAA), Statens Serum Institut [Copenhagen], Immuno-Rhumatologie Moléculaire, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), SANTE/SIDA [Bobo-Dioulasso, Burkina Faso], Institut de Recherche en Sciences de la Santé (IRSS) / Centre Muraz, Department of Microbiology, University of Washington School of Medicine, Department of Microbiology, Medical School, University of Thessaly [Volos] (UTH), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques er émergentes (TransVIHMI), Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Université Montpellier 1 (UM1), Africa Centre for Health and Population Studies, University of KwaZulu-Natal (UKZN)-Medical Research Council of South Africa, Lab-STICC_UBO_CID_IHSEV, Laboratoire des sciences et techniques de l'information, de la communication et de la connaissance (Lab-STICC), École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS)-École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS), State Key Laboratory of Infectious Disease Prevention and Control, Chinese Center for Disease Control and Prevention, Laboratory of Virology, CHU Rouen, Normandie Université (NU)-Normandie Université (NU), Universidade Federal do Rio de Janeiro (UFRJ), Departements of Medicine and Microbiology, University of Alabama [Tuscaloosa] (UA), Stichting HIV Monitoring [Amsterdam], Universiteit van Amsterdam (UvA), Département Génétique Internal Médecine, Hôpital Universitaire Leuven, Department of Chemical and Biomolecular Engineering [Baltimore], Johns Hopkins University (JHU), Centers for Disease Control and Prevention [Atlanta] (CDC), Centers for Disease Control and Prevention, China Academy of Chinese Medical Sciences, Chatzidimitriou, Dimitrios [0000-0001-9656-5898], University of Oxford, Institut Pasteur [Paris] (IP), Istituto Superiore di Sanità (ISS), Microbiologie Fondamentale et Pathogénicité (MFP), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Recherches Translationnelles sur le VIH et les maladies infectieuses endémiques et émergentes (TransVIHMI), Institut de Recherche pour le Développement (IRD)-Université de Yaoundé I-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), University of KwaZulu-Natal [Durban, Afrique du Sud] (UKZN)-Medical Research Council of South Africa, Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS)-Université européenne de Bretagne - European University of Brittany (UEB)-École Nationale d'Ingénieurs de Brest (ENIB)-Université de Bretagne Sud (UBS)-Université de Brest (UBO)-Télécom Bretagne-Institut Brestois du Numérique et des Mathématiques (IBNM), Université de Brest (UBO)-École Nationale Supérieure de Techniques Avancées Bretagne (ENSTA Bretagne)-Institut Mines-Télécom [Paris] (IMT)-Centre National de la Recherche Scientifique (CNRS), UNAIDS, Noguchi Memorial Institute for Medical Research, University of Ghana, Laboratoire d'Electronique et des Technologies de l'Information (CEA-LETI), Université Grenoble Alpes (UGA)-Direction de Recherche Technologique (CEA) (DRT (CEA)), Beihang University, Recherches Translationnelles sur le VIH et les maladies infectieuses (TransVIHMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Recherche pour le Développement (IRD)-Université Montpellier 1 (UM1)-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Universtié Yaoundé 1 [Cameroun]-Université de Montpellier (UM), Universidade Federal do Rio de Janeiro [Rio de Janeiro] (UFRJ), Nuffield Department of Women's and Reproductive Health (NDWRH), University of Oxford- John Radcliffe Hospital [Oxford University Hospital], South African Centre for Epidemiological Modelling and Analysis, JH is supported by the Oxford University Clinical Academic Graduate School (Oxford, UK) and Linacre College, Oxford University (Oxford, UK)., WHO–UNAIDS Network for HIV Isolation Characterisation : Alash'le G Abimiku, Simon Agwale, Chris Archibald, Boaz Avidor, María Gabriela Barbás, Francoise Barre-Sinoussi, Banson Barugahare, El Hadj Belabbes, Silvia Bertagnolio, Deborah Birx, Aleksei F Bobkov, James Brandful, Helba Bredell, Catherine A Brennan, James Brooks, Marie Bruckova, Luigi Buonaguro, Franco Buonaguro, Stefano Buttò, Anne Buve, Mary Campbell, Jean Carr, Alex Carrera, Manuel Gómez Carrillo, Connie Celum, Beth Chaplin, Macarthur Charles, Dimitrios Chatzidimitriou, Zhiwei Chen, Katsumi Chijiwa, David Cooper, Philip Cunningham, Anoumou Dagnra, Cillian F de Gascun, Julia Del Amo, Elena Delgado, Ursula Dietrich, Dominic Dwyer, Dennis Ellenberger, Barbara Ensoli, Max Essex, Feng Gao, Herve Fleury, Peter N Fonjungo, Vincent Foulongne, Deepak A Gadkari, Federico García, Roger Garsia, Guy Michel Gershy-Damet, Judith R Glynn, Ruth Goodall, Zehava Grossman, Monick Lindenmeyer-Guimarães, Beatrice Hahn, Raph L Hamers, Osamah Hamouda, Ray Handema, Xiang He, Joshua Herbeck, David D Ho, Africa Holguin, Mina Hosseinipour, Gillian Hunt, Masahiko Ito, Mohamed Ali Bel Hadj Kacem, Erin Kahle, Pontiano Kaleebu Kaleebu, Marcia Kalish, Adeeba Kamarulzaman, Chun Kang, Phyllis Kanki, Edward Karamov, Jean-Claude Karasi, Kayitesi Kayitenkore, Tony Kelleher, Dwip Kitayaporn, Leondios G Kostrikis, Claudia Kucherer, Claudia Lara, Thomas Leitner, Kirsi Liitsola, Jai Lingappa, Marek Linka, Ivette Lorenzana de Rivera, Vladimir Lukashov, Shlomo Maayan, Luzia Mayr, Francine McCutchan, Nicolas Meda, Elisabeth Menu, Fred Mhalu, Doreen Mloka, John L Mokili, Brigitte Montes, Orna Mor, Mariza Morgado, Fausta Mosha, Awatef Moussi, James Mullins, Rafael Najera, Mejda Nasr, Nicaise Ndembi, Joel R Neilson, Vivek R Nerurkar, Florian Neuhann, Claudine Nolte, Vlad Novitsky, Philippe Nyambi, Marianna Ofner, Fem J Paladin, Anna Papa, Jean Pape, Neil Parkin, Chris Parry, Martine Peeters, Alexandra Pelletier, Lucía Pérez-Álvarez, Deenan Pillay, Angie Pinto, Trinh Duy Quang, Cecilia Rademeyer, Filimone Raikanikoda, Mark A Rayfield, Jean-Marc Reynes, Tobias Rinke de Wit, Kenneth E Robbins, Morgane Rolland, Christine Rousseau, Jesus Salazar-Gonzales, Hanan Salem, Mika Salminen, Horacio Salomon, Paul Sandstrom, Mario L Santiago, Abdoulaye D Sarr, Bryan Schroeder, Michel Segondy, Philippe Selhorst, Sylvester Sempala, Jean Servais, Ansari Shaik, Yiming Shao, Amine Slim, Marcelo A Soares, Elijah Songok, Debbie Stewart, Julie Stokes, Shambavi Subbarao, Ruengpung Sutthent, Jun Takehisa, Amilcar Tanuri, Kok Keng Tee, Kiran Thapa, Michael Thomson, Tyna Tran, Willy Urassa, Hiroshi Ushijima, Philippevan de Perre, Guidovan der Groen, Kristel van Laethem, Joep van Oosterhout, Ard van Sighem, Eric van Wijngaerden, Anne-Mieke Vandamme, Jurgen Vercauteren, Nicole Vidal, Lesley Wallace, Carolyn Williamson, Dawit Wolday, Jianqing Xu, Chunfu Yang, Linqi Zhang, and Rong Zhang

Subjects
0301 basic medicine, Serotype, Genotype, Genotyping Techniques, 030106 microbiology, DIVERSITY, MULTICENTER, VACCINE, HIV Infections, Genome, Viral, Biology, Global Health, Serogroup, SUBTYPES, 03 medical and health sciences, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Surveys and Questionnaires, INFECTION, Genetic variation, Global health, Humans, HIV vaccine, Serotyping, AIDS Vaccines, Science & Technology, Molecular epidemiology, Genetic Variation, Subtyping, 3. Good health, Trend analysis, 030104 developmental biology, Infectious Diseases, 13. Climate action, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, HIV-1, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Life Sciences & Biomedicine, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Demography
Abstract

BACKGROUND: Global genetic diversity of HIV-1 is a major challenge to the development of HIV vaccines. We aimed to estimate the regional and global distribution of HIV-1 subtypes and recombinants during 1990-2015. METHODS: We searched PubMed, EMBASE (Ovid), CINAHL (Ebscohost), and Global Health (Ovid) for HIV-1 subtyping studies published between Jan 1, 1990, and Dec 31, 2015. We collected additional unpublished HIV-1 subtyping data through a global survey. We included prevalence studies with HIV-1 subtyping data collected during 1990-2015. We grouped countries into 14 regions and analysed data for four time periods (1990-99, 2000-04, 2005-09, and 2010-15). The distribution of HIV-1 subtypes, circulating recombinant forms (CRFs), and unique recombinant forms (URFs) in individual countries was weighted according to the UNAIDS estimates of the number of people living with HIV (PLHIV) in each country to generate regional and global estimates of HIV-1 diversity in each time period. The primary outcome was the number of samples designated as HIV-1 subtypes A, B, C, D, F, G, H, J, K, CRFs, and URFs. The systematic review is registered with PROSPERO, number CRD42017067164. FINDINGS: This systematic review and global survey yielded 2203 datasets with 383 519 samples from 116 countries in 1990-2015. Globally, subtype C accounted for 46·6% (16 280 897/34 921 639 of PLHIV) of all HIV-1 infections in 2010-15. Subtype B was responsible for 12·1% (4 235 299/34 921 639) of infections, followed by subtype A (10·3%; 3 587 003/34 921 639), CRF02_AG (7·7%; 2 705 110/34 921 639), CRF01_AE (5·3%; 1 840 982/34 921 639), subtype G (4·6%; 1 591 276/34 921 639), and subtype D (2·7%; 926 255/34 921 639). Subtypes F, H, J, and K combined accounted for 0·9% (311 332/34 921 639) of infections. Other CRFs accounted for 3·7% (1 309 082/34 921 639), bringing the proportion of all CRFs to 16·7% (5 844 113/34 921 639). URFs constituted 6·1% (2 134 405/34 921 639), resulting in recombinants accounting for 22·8% (7 978 517/34 921 639) of all global HIV-1 infections. The distribution of HIV-1 subtypes and recombinants changed over time in countries, regions, and globally. At a global level during 2005-15, subtype B increased, subtypes A and D were stable, and subtypes C and G and CRF02_AG decreased. CRF01_AE, other CRFs, and URFs increased, leading to a consistent increase in the global proportion of recombinants over time. INTERPRETATION: Global and regional HIV diversity is complex and evolving, and is a major challenge to HIV vaccine development. Surveillance of the global molecular epidemiology of HIV-1 remains crucial for the design, testing, and implementation of HIV vaccines. FUNDING: None. ispartof: LANCET INFECTIOUS DISEASES vol:19 issue:2 pages:143-155 ispartof: location:United States status: published

Published
2018

49. Origin of AIDS: Contaminated polio vaccine theory refuted

Author

Worobey, Michael, Santiago, Mario L., Keele, Brandon F., Ndjango, Jean-Bosco N., Joy, Jeffrey B., Labama, Bernard L., Dhed'a, Benoît D., Rambaut, Andrew, Sharp, Paul M., Shaw, George M., and Hahn, Beatrice H.

Published
2004

50. SIVcpz in Wild Chimpanzees

Author

Santiago, Mario L., Rodenburg, Cynthia M., Kamenya, Shadrack, Bibollet-Ruche, Frederic, Gao, Feng, Bailes, Elizabeth, Meleth, Sreelatha, Soong, Seng-Jaw, Kilby, J. Michael, Moldoveanu, Zina, Fahey, Babette, Muller, Martin N., Ayouba, Ahidjo, Nerrienet, Eric, McClure, Harold M., Heeney, Jonathan L., Pusey, Anne E., Collins, D. Anthony, Boesch, Christophe, Wrangham, Richard W., Goodall, Jane, Sharp, Paul M., Shaw, George M., and Hahn, Beatrice H.

Published
2002

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