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

Author

Dawit Wolday, Neil Parkin, Bryan Schroeder, Mary S. Campbell, Barbara Ensoli, Jean-Claude Karasi, Connie Celum, Ard van Sighem, Marcia L. Kalish, Gillian Hunt, Jurgen Vercauteren, Dimitrios Chatzidimitriou, Beth Chaplin, Alex Carrera, Ruth L. Goodall, Guido van der Groen, Martine Peeters, Leondios G. Kostrikis, Edward Karamov, Francine E. McCutchan, Cecilia Rademeyer, Mina C. Hosseinipour, Michael M. Thomson, Fred Mhalu, Christopher M. Parry, Florian Neuhann, Jean-Marc Reynes, James I. Mullins, Vivek R. Nerurkar, Pontiano Kaleebu, Phyllis J. Kanki, Christine Rousseau, Deepak A Gadkari, Luzia Mayr, Kristel Van Laethem, Vincent Foulongne, Guy Michel Gershy-Damet, Lesley Wallace, Mika Salminen, Carolyn Williamson, John L. Mokili, África Holguín, Horacio Salomon, James Brandful, Alexandra Pelletier, Philippe Van de Perre, Xiang He, Tyna Tran, Marie Bruckova, Jianqing Xu, Monick Lindenmeyer-Guimarães, Stefano Buttò, Anoumou Y. Dagnra, Deenan Pillay, Doreen Mloka, Aleksei F Bobkov, Mejda Nasr, Ivette Lorenzana de Rivera, Kenneth E. Robbins, Elisabeth Menu, Ruengpung Sutthent, María Gabriela Barbás, Hervé Fleury, Joep J. van Oosterhout, Rong Zhang, Luigi Buonaguro, Linqi Zhang, David D. Ho, Kayitesi Kayitenkore, Chris P. Archibald, Mario L. Santiago, Dennis Ellenberger, Boaz Avidor, Peter N. Fonjungo, Claudine Nolte, Nicole Vidal, Silvia Bertagnolio, Mohamed Ali Bel Hadj Kacem, Philippe Nyambi, Marianna Ofner, Abdoulaye Dieng Sarr, Rafael Nájera, Chun Kang, Claudia Kücherer, Manuel Gómez Carrillo, El Hadj Belabbes, Simon Agwale, Zhiwei Chen, Zehava Grossman, Dominic M. Dwyer, Eric Van Wijngaerden, Jean W. Pape, Beatrice H. Hahn, Angie N Pinto, Tobias F. Rinke de Wit, Lucía Pérez-Álvarez, Peter D. Ghys, Franco M. Buonaguro, Sylvester Sempala, Vlad Novitsky, Banson Barugahare, Judith R. Glynn, Jason Yun, Macarthur Charles, Katsumi Chijiwa, Kok Keng Tee, Julia del Amo, Adeeba Kamarulzaman, Federico García, Awatef Moussi, Elena Delgado, Hiroshi Ushijima, Shambavi Subbarao, Ray Handema, Catherine A. Brennan, Paul Sandstrom, David A. Cooper, Joel R. Neilson, Ramyiadarsini Elangovan, Dwip Kitayaporn, Claudia Lara, Max Essex, Osamah Hamouda, Anna Papa, Hanan Salem, Elijah M. Songok, Fausta Mosha, Helba Bredell, Shlomo Maayan, Joshua T. Herbeck, Yiming Shao, Ansari Shaik, Kiran Thapa, Jean K. Carr, Raph L. Hamers, Chunfu Yang, Feng Gao, Orna Mor, Filimone Raikanikoda, Jesus Salazar-Gonzales, Nicolas Meda, Erin M. Kahle, Amilcar Tanuri, Tony Kelleher, Masahiko Ito, Fem J Paladin, J.R. Lingappa, Julie Stokes, Shona Kirtley, Vladimir Lukashov, Anne-Mieke Vandamme, Deborah L. Birx, Philip Cunningham, Amine Slim, Nicaise Ndembi, James Brooks, Alash'le Abimiku, Françoise Barré-Sinoussi, Trinh Duy Quang, Eleanor Gouws-Williams, Mariza G. Morgado, Jun Takehisa, Michel Segondy, Joris Hemelaar, Debbie Stewart, Cillian De Gascun, Marcelo A. Soares, Anne Buvé, Mark A. Rayfield, Marek Linka, Ursula Dietrich, Roger Garsia, Thomas Leitner, Philippe Selhorst, Jean Servais, Morgane Rolland, Kirsi Liitsola, Leslie Dickson-Tetteh, Brigitte Montes, Willy Urassa, Global Health, AII - Infectious diseases, Graduate School, Experimental Immunology, APH - Personalized Medicine, APH - Quality of Care, Nuffield Department of Population Health [Oxford], University of Oxford [Oxford], John Radcliffe Hospital [Oxford University Hospital], UNAIDS [Genève, Suisse] (ONUSIDA), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Pathogénèse et contrôle des infections chroniques (PCCI), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre Hospitalier Universitaire de Montpellier (CHU Montpellier )

Subjects
0301 basic medicine, medicine.medical_specialty, Genotype, Epidemiology, Immunology, HIV Infections, MESH: Global Health, Global Health, MESH: Genotype, MESH: HIV-1, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Virology, Global health, medicine, Humans, MESH: Molecular Epidemiology, 030212 general & internal medicine, MESH: Genetic Variation, HIV vaccine, CRFS, Molecular Epidemiology, MESH: Humans, Molecular epidemiology, business.industry, Genetic Variation, virus diseases, MESH: HIV Infections, 030112 virology, Subtyping, 3. Good health, Infectious Diseases, Systematic review, MESH: Reassortant Viruses, HIV-1, [SDV.IMM]Life Sciences [q-bio]/Immunology, business, Viral load, Reassortant Viruses, Demography
Abstract

International audience; Background: Global HIV-1 genetic diversity and evolution form a major challenge to treatment and prevention efforts. An increasing number of distinct HIV-1 recombinants have been identified worldwide, but their contribution to the global epidemic is unknown. We aimed to estimate the global and regional distribution of HIV-1 recombinant forms during 1990-2015.Methods: We assembled a global HIV-1 molecular epidemiology database through a systematic literature review and a global survey. We searched the PubMed, Embase (Ovid), CINAHL (Ebscohost), and Global Health (Ovid) databases for HIV-1 subtyping studies published from Jan 1, 1990, to Dec 31, 2015. Unpublished original HIV-1 subtyping data were collected through a survey among experts in the field who were members of the WHO-UNAIDS Network for HIV Isolation and Characterisation. We included prevalence studies with HIV-1 subtyping data collected during 1990-2015. Countries were grouped into 14 regions and analyses were done for four time periods (1990-99, 2000-04, 2005-09, and 2010-15). The distribution of 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 in each country to generate regional and global estimates of numbers and proportions of HIV-1 recombinants in each time period. The systematic review is registered with PROSPERO, CRD42017067164.Findings: Our global data collection yielded an HIV-1 molecular epidemiology database of 383 519 samples from 116 countries in 1990-2015. We found that the proportion of recombinants increased over time, both globally and in most regions, reaching 22·8% (7 978 517 of 34 921 639) of global HIV-1 infections in 2010-15. Both the proportion and the number of distinct CRFs detected increased over time to 16·7% and 57 CRFs in 2010-15. The global and regional distribution of HIV-1 recombinants was diverse and evolved over time, and we found large regional variation in the numbers (0-44 CRFs), types (58 distinct CRFs), and proportions (0-80·5%) of HIV-1 recombinants. Globally, CRF02_AG was the most prevalent recombinant, accounting for 33·9% (2 701 364 of 7 978 517) of all recombinant infections in 2010-15. URFs accounted for 26·7% (2 131 450 of 7 978 517), CRF01_AE for 23·0% (1 838 433), and other CRFs for 16·4% (1 307 270) of all recombinant infections in 2010-15. Although other CRFs accounted for small proportions of infections globally (

Published
2020
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2. The HIV-1 integrase-LEDGF allosteric inhibitor MUT-A: resistance profile, impairment of virus maturation and infectivity but without influence on RNA packaging or virus immunoreactivity

Author

François Moreau, Sophie Chasset, Felipe García, Marc Ruff, Ben Berkhout, Erwann Le Rouzic, Danièle Spehner, Benoit Ledoussal, Laia Miralles, Stéphane Emiliani, Francis Chevreuil, Igor Orlov, Alessia Zamborlini, Christiane Moog, Julie Brias, Bruno P. Klaholz, Nikki van Bel, Céline Amadori, José M. Gatell, Damien Bonnard, Luzia Mayr, Yme U. van der Velden, Richard Benarous, Montserrat Plana, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Les Laboratoires Biodim-Mutabilis [Romainville], Biocitech, Université Sorbonne Paris Cité (USPC), Laboratory of Experimental Virology - Department of Medical Microbiology [Amsterdam, The Netherlands], Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA)-University of Amsterdam [Amsterdam] (UvA)-Center for Infection and Immunity Amsterdam - CINIMA [Amsterdam, The Netherlands], Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), AIDS Research Group [Barcelona, Spain], Hospital Clinic [Barcelona, Spain]-August Pi i Sunyer Biomedical Research Institute - IDIBAPS [Barcelona, Spain], Immuno-Rhumatologie Moléculaire, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Pathologie cellulaire : aspects moléculaires et viraux / Pathologie et Virologie Moléculaire, Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS), This work was supported by Biodim Mutabilis under the Authorization Number DUO 2145, assigned by the French Ministry of Research for work with genetically modified organisms, and by Grants from EU FP7 to Biodim, BB, SE and AZ under the HIVINNOV consortium, Grant Agreement No. 305137, from the Eurostar Grant ResistAids to Biodim and BB (Grant Agreement No. E!10239) and by the French Infrastructure for Integrated Structural Biology (FRISBI) ANR-10-INSB-05-01, and Instruct as part of the European Strategy Forum on Research Infrastructures (ESFRI). Felipe García team was supported by Grants SAF2015-66193-R, SAF2012-39075, Montserrat Plana by Grant FIS PI15/00480 and Nikki van Bel by NWO-CW (TOP Grant)., ANR-10-INBS-0005,FRISBI,Infrastructure Française pour la Biologie Structurale Intégrée(2010), European Project: 305137,EC:FP7:HEALTH,FP7-HEALTH-2012-INNOVATION-1,HIVINNOV(2012), Les Laboratoires Biodim-Mutabilis, Centre d'Economie de l'Université Paris Nord (CEPN), Université Paris 13 (UP13)-Université Sorbonne Paris Cité (USPC)-Centre National de la Recherche Scientifique (CNRS), Génomes, biologie cellulaire et thérapeutiques (GenCellDi (UMR_S_944)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Collège de France (CdF (institution))-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Institut Cochin (UMR_S567 / UMR 8104), Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Center for Infection and Immunity Amsterdam (CINIMA), August Pi i Sunyer Biomedical Research Institute - IDIBAPS [Barcelona, Spain]-Hospital Clinic [Barcelona, Spain], Collège de France (CdF (institution))-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Collège de France (CdF)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5), Immunorhumathologie moléculaire, Institut National de la Santé et de la Recherche Médicale (INSERM), ANR-10-INBS-05-01/10-INBS-0005,FRISBI,Infrastructure Française pour la Biologie Structurale Intégrée(2010), Klaholz, Bruno, Infrastructure Française pour la Biologie Structurale Intégrée - - FRISBI2010 - ANR-10-INBS-0005 - INBS - VALID, Generation of a new class of antiretrovirals targeting HIV-cellular cofactors interactions - HIVINNOV - - EC:FP7:HEALTH2012-10-01 - 2015-09-30 - 305137 - VALID, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Centre National de la Recherche Scientifique (CNRS), AII - Infectious diseases, Medical Microbiology and Infection Prevention, and Amsterdam institute for Infection and Immunity

Subjects
0301 basic medicine, lcsh:Immunologic diseases. Allergy, Pyridines, Virus Integration, T cell, [SDV]Life Sciences [q-bio], Aucun, HIV Integrase, Thiophenes, Allosteric integrase inhibitor, HIV Antibodies, Virus Replication, Integrase, Virus, Cell Line, 03 medical and health sciences, INLAI, Immunoreactivity, Virology, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, medicine, Virus maturation, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, LEDGIN, HIV Integrase Inhibitors, LEDGF, Infectivity, biology, Research, Virus Assembly, RNA, virus diseases, Group-specific antigen, Reverse transcriptase, 3. Good health, [SDV] Life Sciences [q-bio], 030104 developmental biology, Infectious Diseases, medicine.anatomical_structure, biology.protein, HIV-1, Intercellular Signaling Peptides and Proteins, lcsh:RC581-607
Abstract

Background HIV-1 Integrase (IN) interacts with the cellular co-factor LEDGF/p75 and tethers the HIV preintegration complex to the host genome enabling integration. Recently a new class of IN inhibitors was described, the IN-LEDGF allosteric inhibitors (INLAIs). Designed to interfere with the IN-LEDGF interaction during integration, the major impact of these inhibitors was surprisingly found on virus maturation, causing a reverse transcription defect in target cells. Results Here we describe the MUT-A compound as a genuine INLAI with an original chemical structure based on a new type of scaffold, a thiophene ring. MUT-A has all characteristics of INLAI compounds such as inhibition of IN-LEDGF/p75 interaction, IN multimerization, dual antiretroviral (ARV) activities, normal packaging of genomic viral RNA and complete Gag protein maturation. MUT-A has more potent ARV activity compared to other INLAIs previously reported, but similar profile of resistance mutations and absence of ARV activity on SIV. HIV-1 virions produced in the presence of MUT-A were non-infectious with the formation of eccentric condensates outside of the core. In studying the immunoreactivity of these non-infectious virions, we found that inactivated HIV-1 particles were captured by anti-HIV-specific neutralizing and non-neutralizing antibodies (b12, 2G12, PGT121, 4D4, 10-1074, 10E8, VRC01) with efficiencies comparable to non-treated virus. Autologous CD4+ T lymphocyte proliferation and cytokine induction by monocyte-derived dendritic cells (MDDC) pulsed either with MUT-A-inactivated HIV or non-treated HIV were also comparable. Conclusions Although strongly defective in infectivity, HIV-1 virions produced in the presence of the MUT-A INLAI have a normal protein and genomic RNA content as well as B and T cell immunoreactivities comparable to non-treated HIV-1. These inactivated viruses might form an attractive new approach in vaccine research in an attempt to study if this new type of immunogen could elicit an immune response against HIV-1 in animal models. Electronic supplementary material The online version of this article (10.1186/s12977-017-0373-2) contains supplementary material, which is available to authorized users.

Published
2017
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3. Role of nonneutralizing antibodies in vaccines and/or HIV infected individuals

Author

Bin Su, Christiane Moog, and Luzia Mayr

Subjects
0301 basic medicine, Immunology, Human immunodeficiency virus (HIV), HIV Infections, HIV Antibodies, Biology, medicine.disease_cause, Virus, Neutralization, 03 medical and health sciences, 0302 clinical medicine, Mediator, Viral entry, Virology, Hiv infected, medicine, Animals, Humans, AIDS Vaccines, Oncology (nursing), Hematology, Antibodies, Neutralizing, 030104 developmental biology, Infectious Diseases, Oncology, HIV-1, biology.protein, Antibody, Viral load, 030215 immunology
Abstract

PURPOSE OF REVIEW Increased body of evidence gathered over time indicate that antibodies are capable of many inhibitory mechanisms, virus neutralization being just one of them. Nonneutralizing antibodyactivities interfering with HIV replication can also lead to a decrease in viral load and even in-vivo protection. RECENT FINDINGS It was previously believed that neutralizing antibodies can achieve sterilizing protection mainly by using their neutralization capacities against the infecting virus directly at the portal of virus entry. Recent findings show that protection can be obtained by neutralizing antibodiesat distal sites of virus challenge. In this case, foci of virus infection that escaped from initial inhibition of virus are eliminated presumably by additional nonneutralizing antibody activities. These data inexorably strengthen the diverse functions of antibodies and broaden their role as antiviral mediator. SUMMARY The review summarizes the current knowledge and the difficulties to encompass the numerous functions of antibodies. A complete understanding of the various facets of antibody functions is required to efficiently induce them via next-generation vaccine design.

Published
2017
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4. Contrasting antibody responses to intrasubtype superinfection with CRF02_AG

Author

Luzia Mayr, Michael Tuen, Lydia Sykora, Ralf Dürr, Andrew N. Banin, Aubin Nanfack, Daniel Bruno, Xunqing Jiang, Xiang-Peng Kong, Colleen R. Courtney, Allison R. Kirkpatrick, Craig Martens, Phillipe N. Nyambi, Ruimin Pan, Andrew D. Redd, Stephen F. Porcella, and Thomas C. Quinn

Subjects
0301 basic medicine, RNA viruses, Physiology, viruses, HIV Infections, medicine.disease_cause, Pathology and Laboratory Medicine, Biochemistry, Neutralization, Database and Informatics Methods, Epitopes, Immunodeficiency Viruses, Pregnancy, Immune Physiology, Medicine and Health Sciences, Neutralizing antibody, Immune Response, Phylogeny, Recombination, Genetic, Multidisciplinary, Immune System Proteins, biology, env Gene Products, Human Immunodeficiency Virus, virus diseases, Viral Load, 3. Good health, Infectious Diseases, Medical Microbiology, Superinfection, Viral Pathogens, Viruses, Medicine, Female, Antibody, Pathogens, Viral load, Sequence Analysis, Research Article, Bioinformatics, Science, Immunology, HIV superinfection, Research and Analysis Methods, Microbiology, Virus, Antibodies, 03 medical and health sciences, Viral envelope, Amino Acid Sequence Analysis, Retroviruses, parasitic diseases, medicine, Genetics, Humans, Microbial Pathogens, Evolutionary Biology, Population Biology, Lentivirus, Organisms, Biology and Life Sciences, HIV, Proteins, biochemical phenomena, metabolism, and nutrition, Virology, Antibodies, Neutralizing, 030104 developmental biology, pol Gene Products, Human Immunodeficiency Virus, Antibody Formation, biology.protein, HIV-1, Sequence Alignment, Population Genetics
Abstract

HIV superinfection describes the sequential infection of an individual with two or more unrelated HIV strains. Intersubtype superinfection has been shown to cause a broader and more potent heterologous neutralizing antibody response when compared to singly infected controls, yet the effects of intrasubtype superinfection remain controversial. Longitudinal samples were analyzed phylogenetically for pol and env regions using Next-Generation Sequencing and envelope cloning. The impact of CRF02_AG intrasubtype superinfection was assessed for heterologous neutralization and antibody binding responses. We compared two cases of CRF02_AG intrasubtype superinfection that revealed complete replacement of the initial virus by superinfecting CRF02_AG variants with signs of recombination. NYU6564, who became superinfected at an early time point, exhibited greater changes in antibody binding profiles and generated a more potent neutralizing antibody response post-superinfection compared to NYU6501. In contrast, superinfection occurred at a later time point in NYU6501 with strains harboring significantly longer V1V2 regions with no observable changes in neutralization patterns. Here we show that CRF02_AG intrasubtype superinfection can induce a cross-subtype neutralizing antibody response, and our data suggest timing and/or superinfecting viral envelope characteristics as contributing factors. These results highlight differential outcomes in intrasubtype superinfection and provide the first insight into cases with CRF02_AG, the fourth most prevalent HIV-1 strain worldwide.

Published
2017

5. Neuropilin-1 Expression on Regulatory T Cells Enhances Their Interactions with Dendritic Cells during Antigen Recognition

Author

Kristian G. Andersen, Alexander G. Betz, Felix Randow, Milka Sarris, and Luzia Mayr

Subjects
Immunology, Antigen presentation, Receptors, Antigen, T-Cell, chemical and pharmacologic phenomena, Cell Communication, Biology, T-Lymphocytes, Regulatory, Mice, Transduction, Genetic, Animals, Immunology and Allergy, Cytotoxic T cell, IL-2 receptor, MOLIMMUNO, Antigen-presenting cell, Antigen Presentation, CD40, Reverse Transcriptase Polymerase Chain Reaction, Histocompatibility Antigens Class II, CD28, Dendritic Cells, T-Lymphocytes, Helper-Inducer, Flow Cytometry, Natural killer T cell, Acquired immune system, Immunohistochemistry, Neuropilin-1, Infectious Diseases, CELLIMMUNO, biology.protein
Abstract

SUMMARY The interaction of T cells with dendritic cells (DCs) determines whether an immune response is launched or not. Recognition of antigen leads to formation of immunological synapses at the interface between the cells. The length of interaction is likely to determine the functional outcome, because it limits the number of MHC class II-peptide complexes that can be recruited into the synapse. Here, we show that regulatory T (Treg) cells and naive helper T (Th) cells interact differently with DCs in the absence of proinflammatory stimuli. Although differences in T cell receptor repertoire might contribute, Foxp3induced phenotypic differences play a major role. We found that Neuropilin-1 (Nrp-1), which is expressed by most Treg cells but not naive Th cells, promoted prolonged interactions with immature DCs (iDCs), resulting in higher sensitivity to limiting amounts of antigen. This is likely to give Treg cells an advantage over naive Th cells, with the same specificity leading to a ‘‘default’’ suppression of immune responses in the absence of ‘‘danger signals.’’

Published
2008
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6. Epitope mapping of conformational V2-specific anti-HIV human monoclonal antibodies reveals an immunodominant site in V2

Author

Brett Spurrier, Sandra Cohen, Xiang-Peng Kong, Susan Zolla-Pazner, and Luzia Mayr

Subjects
Models, Molecular, Protein Conformation, Immunoglobulin Variable Region, lcsh:Medicine, Plasma protein binding, HIV Antibodies, HIV Envelope Protein gp120, Epitope, Epitopes, 0302 clinical medicine, Protein structure, lcsh:Science, chemistry.chemical_classification, 0303 health sciences, Multidisciplinary, biology, Vaccination, Antibodies, Monoclonal, 3. Good health, Subviral Particles, 030220 oncology & carcinogenesis, Medicine, Infectious diseases, Antibody, Protein Binding, Research Article, medicine.drug_class, Molecular Sequence Data, Immunology, HIV prevention, Viral diseases, Viral Structure, Monoclonal antibody, Microbiology, Cell Line, 03 medical and health sciences, Virology, Vaccine Development, medicine, Humans, Amino Acid Sequence, Binding site, Biology, 030304 developmental biology, Binding Sites, lcsh:R, Immunity, HIV, Molecular biology, Epitope mapping, chemistry, Mutation, biology.protein, HIV-1, lcsh:Q, Clinical Immunology, Glycoprotein, Epitope Mapping
Abstract

In the case-control study of the RV144 vaccine trial, the levels of antibodies to the V1V2 region of the gp120 envelope glycoprotein were found to correlate inversely with risk of HIV infection. This recent demonstration of the potential role of V1V2 as a vaccine target has catapulted this region into the focus of HIV-1 research. We previously described seven human monoclonal antibodies (mAbs) derived from HIV-infected individuals that are directed against conformational epitopes in the V1V2 domain. In this study, using lysates of SF162 pseudoviruses carrying V1V2 mutations, we mapped the epitopes of these seven mAbs. All tested mAbs demonstrated a similar binding pattern in which three mutations (F176A, Y177T, and D180L) abrogated binding of at least six of the seven mAbs to ≤15% of SF162 wildtype binding. Binding of six or all of the mAbs was reduced to ≤50% of wildtype by single substitutions at seven positions (168, 180, 181, 183, 184, 191, and 193), while one change, V181I, increased the binding of all mAbs. When mapped onto a model of V2, our results suggest that the epitope of the conformational V2 mAbs is located mostly in the disordered region of the available crystal structure of V1V2, overlapping and surrounding the α4β7 binding site on V2.

Published
2013

7. Genetic variability and drug resistance mutations in HIV-1 infected individuals on HAART or drug naïve in Limbe, Cameroon

Author

Phillipe N. Nyambi, Luzia Mayr, L Agyingi, T Kinge, D Barengolts, and M MBida

Subjects
Genetics, lcsh:Immunologic diseases. Allergy, education.field_of_study, Genetic diversity, Population, virus diseases, Drug resistance, Biology, Virology, Reverse transcriptase, Infectious Diseases, Poster Presentation, Genotype, Genetic variability, education, lcsh:RC581-607, Gene, Nested polymerase chain reaction
Abstract

Background Cameroon is a country in West Central Africa with a population of about 20 million inhabitants, with an estimated HIV prevalence of 5.1% in the general population. The HIV epidemic in this region is marked by a broad genetic diversity dominated by Circulating Recombinant Forms (CRFs). Methods To characterize HIV-1 genotypes circulating in HIV positive individuals in Limbe, Cameroon, we phylogenetically analyzed blood samples from 116 HIV positive patients. Of 116 samples tested, 110 were amplified by nested PCR at the Gag, Pol and Env genes. Sequences obtained were phylogenetically analyzed with reference sequences from the Los Alamos database. The RT region of samples was also amplified to identify mutations that conferred resistance to Reverse Transcriptase inhibitors (RTIs) using the Stanford University Drug resistance database. Results

Published
2012

8. Superinfection by discordant subtypes of HIV-1 does not enhance the neutralizing antibody response against autologous virus

Author

Arthur Nádas, JN Ngai, Luzia Mayr, Rebecca L.R. Powell, and Phillipe N. Nyambi

Subjects
lcsh:Immunologic diseases. Allergy, biology, business.industry, viruses, virus diseases, Heterologous, biochemical phenomena, metabolism, and nutrition, medicine.disease_cause, Virology, Virus, Immune system, Infectious Diseases, Antigen, Superinfection, Immunology, Poster Presentation, medicine, biology.protein, Antibody, business, Neutralizing antibody, lcsh:RC581-607, Subtypes of HIV
Abstract

Background Recent studies have demonstrated that both the potency and breadth of the humoral anti-HIV-1 immune response in generating neutralizing antibodies (nAbs) against heterologous viruses are significantly enhanced after superinfection by discordant HIV-1 subtypes, suggesting that repeated exposure of the immune system to highly diverse HIV-1 antigens can significantly improve anti-HIV-1 immunity. We investigated whether sequential plasma from subjects superinfected with discordant HIV-1 subtypes, who exhibit broad nAbs against heterologous viruses, also neutralize either or both of their discordant early autologous viruses with increasing potency.

Published
2012

9. Sequence Analysis of the Dimerization Initiation Site of Concordant and Discordant Viral Variants Superinfecting HIV Type 1 Patients

Author

Rebecca L.R. Powell, Thompson Kinge, Phillipe N. Nyambi, and Luzia Mayr

Subjects
Sequence analysis, viruses, Immunology, Molecular Sequence Data, Codon, Initiator, HIV Infections, Biology, chemistry.chemical_compound, Phylogenetics, In vivo, Virology, Genetic variation, Humans, Nucleotide, Phylogeny, Genetics, chemistry.chemical_classification, Recombination, Genetic, Base Sequence, Genetic Variation, Sequence Notes, Sequence Analysis, DNA, In vitro, Infectious Diseases, chemistry, Superinfection, HIV-1, Dimerization, Recombination, DNA
Abstract

For HIV recombination to occur, the RNAs from two infecting strains within a cell must dimerize at the dimerization initiation site (DIS). We examined the sequence identity at the DIS (697-731 bp, Hxb2 numbering engine) in patients superinfected with concordant HIV-1 strains and compared them to those with discordant strains. Viral RNA in sequential plasma from four subjects superinfected with subtype-discordant and two subjects superinfected with subtype-concordant HIV-1 strains was extracted, amplified (5' LTR-early gag: 526-1200 bp, Hxb2 numbering engine), sequenced, and analyzed to determine their compatibility for dimerization in vivo. The concordant viruses infecting the two subjects exhibited identical sequences in the 35-bp-long DIS region while sequences from the discordant viruses revealed single nucleotide changes that were located in the DIS loop (715 bp), its flanking nucleotides (710 bp and 717 bp), and the DIS stem (719 bp). Evidence from in vitro experiments demonstrates that these in vivo changes identified can abolish dimerization and reduce recombination frequency. Therefore, these results revealing differences in the DIS of discordant strains versus the similarity noted for the concordant strains may contribute to the differences in the frequency of recombination in patients superinfected with such HIV-1 variants.

Published
2011

11. Superinfected Patient Pseudovirus Exhibits Resistance to Broadly Neutralizing Antibodies, but Sensitivity to Autologous Plasma Post-superinfection

Author

Sonal Soni, Luzia Mayr, Josephine Meli, Ralf Duerr, Johnson Ngai, Colleen Courtney, and Phillipe N. Nyambi

Subjects
biology, viruses, Immunology, virus diseases, Heterologous, Viral quasispecies, medicine.disease_cause, Virology, Glycans and Antibody Effector Functions, Neutralization, law.invention, Infectious Diseases, HIV Antigens, law, Viral evolution, Superinfection, parasitic diseases, biology.protein, Recombinant DNA, medicine, Antibody
Abstract

P34.11 LB Background: Superinfected HIV patients provide the unique opportunity to investigate the immune response after challenge with diverse HIV antigens and remain the major source for recombinant strain production. The competition and/or coexistence of two or more viral strains drive viral evolution and diversity, eventually triggering the generation of more broad and potent neutralizing antibodies (Abs) as compared to singly infected patients. The objective of this study was to analyze the genetic evolution of the viruses found within a superinfected Cameroonian patient, and to determine the neutralization sensitivity of the recombinant viruses to both autologous and heterologous neutralizing Abs. Methods: Longitudinal plasma samples from an HIV-1 superinfected Cameroonian patient were analyzed for their Env diversity, evolution, and recombination events. Pseudoviruses were generated from timepoints before, during, and after superinfection, and were then tested for sensitivity to homologous plasma and to heterologous neutralizing mAbs. Results: Env sequence analysis indicated that the CRF02_AG infected subject became superinfected with an F2 strain resulting in a massive increase in viral diversity. Later, the patient's viral repertoire was narrowed to quasispecies closely clustering with the initial strain. The highest neutralization was observed with autologous plasma from timepoints after superinfection but before the intiation of ART. Of interest, the superinfecting F2 strain was resistant to neutralization with most known broadly neutralizing antibodies (bnAbs) including PG09 and VRC01 while the original infecting CRF02_AG strain was sensitive to these bnAbs. Conclusions: The resistance of the F2 strain to known bnAbs urges the need to generate nAbs from such patients and to monitor the emerging recombinant strains. HIV-1 superinfected patients may serve for the generation of new bnAbs covering multiple subtypes and deliver important knowledge for future vaccine design.

Published
2014
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12. Investigating Broad Neutralization in HIV-1 Non-B Subtype Infection in Yaoundé, Cameroon

Author

Michel C. Nussenzweig, Colleen Courtney, Lilian Nogueira, Luzia Mayr, Susan Zolla-Pazner, Johnson Ngai, Florian Klein, Phillipe N. Nyambi, and Michael S. Seaman

Subjects
chemistry.chemical_classification, biology, business.industry, Immunology, Passive Antibody Functions, Peptide, Acquired immune system, Gp41, Virology, Neutralization, law.invention, Infectious Diseases, Immune system, chemistry, law, Recombinant DNA, biology.protein, Potency, Medicine, Antibody, business
Abstract

P16.03 Background: A hallmark of HIV is its variability, which within group M viruses includes 9 subtypes and over 50 circulating recombinant forms (CRF)s. Cameroon is an epicenter of the disease known for circulation of many subtypes and CRFs, which provides a unique setting to study the immune response to HIV. It is crucial for a successful vaccine to elicit an adaptive immune response against a broad range of viral subtypes. Methods: We have performed subtype analysis of viral RNA isolated from the plasma of 63 HIV-1 infected Cameroonian subjects to verify non-B subtype infection and to monitor for recombination. From the non-B, drug naive cohort, we have isolated IgG (N=264) to screen for neutralization using a tier 2, pseudovirus panel including subtypes A1, B, C, and 01_AE. Samples capable of neutralizing multiple pseudoviruses at high potency were selected for further study to determine neutralization capacity against an extended panel and their ability to bind gp160 envelope peptides. Results: Subtypes A, D, F, G, and K were identified as well as many recombinant forms including the predominant subtype CRF02_AG. The neutralization screen concluded that 9.5% of the IgG samples were able to neutralize at least 2 pseudoviruses at low IgG concentrations. Neutralization of the extended panel revealed that these IgG samples were also able to neutralize 02_AG,G, and AC subtypes. We found that all of the broadly neutralizing IgG samples bound envelope protein gp41, over 80% bound gp120 proteins, 79% bound a scaffolded V1V2 peptide, and 100% of the samples bound cyclic V3 constructs. Conclusions: We have taken the first look at broad neutralization in a cohort infected with non-B subtype viruses and numerous CRFs. IgG from these patients is capable of neutralizing pseudoviruses across clades with high breadth and potency. We have shown that these samples bind strongly to envelope peptides and hope to continue to elucidate how these antibodies are conferring neutralization in order to guide future vaccine design.

Published
2014
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13. Superinfection by Discordant Subtypes of HIV-1 Does Not Enhance the Neutralizing Antibody Response against Autologous Virus

Author

Johnson Ngai, William A. Takang, Luzia Mayr, Rebecca L.R. Powell, Arthur Nádas, and Phillipe N. Nyambi

Subjects
Viral Diseases, viruses, Immunology, lcsh:Medicine, HIV Infections, medicine.disease_cause, Microbiology, Virus, Inhibitory Concentration 50, 03 medical and health sciences, Immunodeficiency Viruses, Antigen, Virology, Vaccine Development, medicine, Humans, Potency, lcsh:Science, Neutralizing antibody, Biology, Immune Response, Phylogeny, Subtypes of HIV, 030304 developmental biology, 0303 health sciences, Multidisciplinary, biology, 030306 microbiology, Vaccination, lcsh:R, Immunity, HIV, virus diseases, Viral Load, Antibodies, Neutralizing, CD4 Lymphocyte Count, 3. Good health, Titer, Infectious Diseases, Superinfection, HIV-1, biology.protein, Medicine, Clinical Immunology, lcsh:Q, Antibody, Research Article
Abstract

Recent studies have demonstrated that both the potency and breadth of the humoral anti-HIV-1 immune response in generating neutralizing antibodies (nAbs) against heterologous viruses are significantly enhanced after superinfection by discordant HIV-1 subtypes, suggesting that repeated exposure of the immune system to highly diverse HIV-1 antigens can significantly improve anti-HIV-1 immunity. Thus, we investigated whether sequential plasma from these subjects superinfected with discordant HIV-1 subtypes, who exhibit broad nAbs against heterologous viruses, also neutralize their discordant early autologous viruses with increasing potency. Comparing the neutralization capacities of sequential plasma obtained before and after superinfection of 4 subjects to those of matched plasma obtained from 4 singly infected control subjects, no difference in the increase in neutralization capacity was observed between the two groups (p = 0.328). Overall, a higher increase in neutralization over time was detected in the singly infected patients (mean change in IC(50) titer from first to last plasma sample: 183.4) compared to the superinfected study subjects (mean change in IC(50) titer from first to last plasma sample: 66.5). Analysis of the Breadth-Potency Scores confirmed that there was no significant difference in the increase in superinfected and singly infected study subjects (p = 0.234). These studies suggest that while superinfection by discordant subtypes induces antibodies with enhanced neutralizing breadth and potency against heterologous viruses, the potency to neutralize their autologous viruses is not better than those seen in singly infected patients.

Published
2012
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14. 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
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