ArticleImmunity2016
Innate Lymphoid Cells Are Depleted Irreversibly during Acute HIV-1 Infection in the Absence of Viral Suppression.
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Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
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108citing papers in PubMed, 1 pooled it
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Who cites it
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- The Hitchhiker Guide to CD4Frontiers in immunology · 2021Pooled it
- Tissue-resident-like CD4+ T cells secreting IL-17 control Mycobacterium tuberculosis in the human lung.The Journal of clinical investigation · 2021Trial
- Innate Lymphoid Cells Activation and Transcriptomic Changes in Response to Human Dengue Infection.Frontiers in immunology · 2021Trial
- Different pattern of stool and plasma gastrointestinal damage biomarkers during primary and chronic HIV infection.PloS one · 2019Trial
- Dietary indoles influence the AHR-RORγt axis and mucosal immune homeostasis in ART-treated SIV infection.JCI insight · 2026Article
- Early life group 2 innate lymphoid cells in health and disease.Molecular and cellular pediatrics · 2026Review
- Characterization of innate lymphoid cells in infants with human cytomegalovirus infection.BMC pediatrics · 2025Article
- Dietary Indoles Modulate Gut Barrier Integrity via the AhR-IL-22 Axis in ART-Treated SIV Infection.bioRxiv : the preprint server for biology · 2025Article
- Spatial and functional diversity of innate lymphoid cells in the human female genital tract may contribute to antiviral responses to HIV.Nature immunology · 2025Article
- Female ILCs on the spotlight.Nature immunology · 2025Article
- Persistent Type I Interferon Signaling Impairs Innate Lymphoid Cells During HIV-1 Infection Under Suppressive ART.Viruses · 2025Article
- Immune-mediated strategies to solving the HIV reservoir problem.Nature reviews. Immunology · 2025Review
- Longitudinal analysis of rhesus macaque metabolome during acute SIV infection reveals disruption in broad metabolite classes.Journal of virology · 2025Article
- Innate lymphoid cells in HIV pathogenesis and in the human female genital tract.Current opinion in HIV and AIDS · 2025Review
- Article
- Gut microbiome composition influences immunologic alterations in the blood and gut of HIV-positive and HIV-negative men who have sex with men.Frontiers in immunology · 2025Article
- Dual role for microbial short-chain fatty acids in modifying SIV disease trajectory following anti-α4β7 antibody administration.Annals of medicine · 2024Article
- Differences in HIV-1 reservoir size, landscape characteristics and decay dynamics in acute and chronic treated HIV-1 Clade C infection.medRxiv : the preprint server for health sciences · 2024Article
- IFIH1 (MDA5) is required for innate immune detection of intron-containing RNA expressed from the HIV-1 provirus.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Innate lymphoid cells are activated in HFRS, and their function can be modulated by hantavirus-induced type I interferons.PLoS pathogens · 2024Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
26 authors at 12 institutions in 7 countries.
Henrik N KløverprisKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa; Department of Immunology and Microbiology, University of Copenhagen, 2200 Copenhagen, Denmark. Electronic address: henrik.kloverpris@k-rith.org.
Samuel W KazerRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA; Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139-4307, USA; Institute for Medical Engineering & Science, Massachusetts Institute of Technology, Cambridge, MA 02139-4307, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02139-4307, USA.
Jenny MjösbergCenter for Infectious Medicine, Karolinska Institute, 171 76 Stockholm, Sweden.
Jenniffer M MabukaKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa.
Amanda WellmannKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa.
Zaza NdhlovuHIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa.
Marisa C YadonKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa.
Shepherd NhamoyebondeKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa.
Maximilian MuenchhoffHIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa; Department of Paediatrics, University of Oxford, Oxford OX1 3SY, UK.
Yannick SimoniAgency for Science, Technology and Research (A(∗)STAR), Singapore Immunology Network (SIgN), 138632 Singapore, Singapore.
Frank AnderssonDepartment of Surgery, Inkosi Albert Luthuli Hospital, KwaZulu-Natal, 4058 Durban, South Africa.
Warren KuhnENT department Stanger Hospital, Stanger, KwaZulu Natal, 4450 Durban, South Africa.
Nigel GarrettDepartment of Infectious Diseases, UKZN, 4001 Durban, South Africa; Center for the AIDS Programme of Research in South Africa - CAPRISA, 4001 Durban, South Africa.
Wendy A BurgersDivision of Medical Virology and Institute of Infectious Disease and Molecular Medicine, University of Cape Town, 7925 Cape Town, South Africa.
Philomena KamyaRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA; HIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa.
Karyn PretoriusHIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa.
Krista DongRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA.
Amber MoodleyRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA.
Evan W NewellAgency for Science, Technology and Research (A(∗)STAR), Singapore Immunology Network (SIgN), 138632 Singapore, Singapore.
Victoria KasprowiczKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa.
Salim S Abdool KarimCenter for the AIDS Programme of Research in South Africa - CAPRISA, 4001 Durban, South Africa; Department of Epidemiology, Columbia University, New York, NY 10027, USA.
Philip GoulderHIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa; Department of Paediatrics, University of Oxford, Oxford OX1 3SY, UK.
Alex K ShalekRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA; Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139-4307, USA; Institute for Medical Engineering & Science, Massachusetts Institute of Technology, Cambridge, MA 02139-4307, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02139-4307, USA; Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02138, USA.
Bruce D WalkerRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA; HIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.
Thumbi Ndung'uKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA; HIV Pathogenesis Programme, Doris Duke Medical Research Institute, UKZN, 4001 Durban, South Africa; Max Planck Institute for Infection Biology, 10117 Berlin, Germany.
Alasdair LeslieKwaZulu-Natal Research Institute for Tuberculosis & HIV (K-RITH), University of KwaZulu-Natal (UKZN), 4001 Durban, South Africa; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02139-4307, USA.
University of KwaZulu-Natal · ZARagon Institute of MGH, MIT and Harvard · USAgency for Science, Technology and Research · SGCentre for the AIDS Programme of Research in South Africa · ZAUniversity of Oxford · GBHarvard University · USHoward Hughes Medical Institute · USKarolinska Institutet · SEMassachusetts Institute of Technology · USMax Planck Institute for Infection Biology · DEStanger Hospital · ZAUniversity of Cape Town · ZA
Funding
Pathogenesis of Clade C HIV InfectionR37AI067073 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WALKER, BRUCE D · 2011 to 2020
$6.6MPathogenesis of Clade C HIV InfectionR01AI067073 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WALKER, BRUCE D · 2006 to 2010
$2.9MNIAID NIH HHS R01 AI067073NIAID NIH HHS R37 AI067073NIAID NIH HHS R37AI067073
Abstract
Innate lymphoid cells (ILCs) play a central role in the response to infection by secreting cytokines crucial for immune regulation, tissue homeostasis, and repair. Although dysregulation of these systems is central to pathology, the impact of HIV-1 on ILCs remains unknown. We found that human blood ILCs were severely depleted during acute viremic HIV-1 infection and that ILC numbers did not recover after resolution of peak viremia. ILC numbers were preserved by antiretroviral therapy (ART), but only if initiated during acute infection. Transcriptional profiling during the acute phase revealed upregulation of genes associated with cell death, temporally linked with a strong IFN acute-phase response and evidence of gut barrier breakdown. We found no evidence of tissue redistribution in chronic disease and remaining circulating ILCs were activated but not apoptotic. These data provide a potential mechanistic link between acute HIV-1 infection, lymphoid tissue breakdown, and persistent immune dysfunction.
Indexed as
Acute DiseaseAntiviral AgentsApoptosisCell MovementCells, CulturedChronic DiseaseCohort StudiesGene Expression RegulationHIV-1HIV InfectionsHumansImmunity, InnateInterferon-gammaIntestinesLymphocytesTime FactorsAntiviral AgentsInterferon-gammaHIV-1 infectioninnate lymphoid cells
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