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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.

Original publication

DOI

10.1016/j.immuni.2016.01.006

Type

Journal article

Journal

Immunity

Publication Date

16/02/2016

Volume

44

Pages

391 - 405

Keywords

HIV-1 infection, innate lymphoid cells, Acute Disease, Antiviral Agents, Apoptosis, Cell Movement, Cells, Cultured, Chronic Disease, Cohort Studies, Gene Expression Regulation, HIV Infections, HIV-1, Humans, Immunity, Innate, Interferon-gamma, Intestines, Lymphocytes, Time Factors, Treatment Outcome, Viral Load