Hypoxic microenvironment shapes HIV-1 replication and latency.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
14 07 2020
Historique:
received: 27 10 2019
accepted: 17 06 2020
entrez: 16 7 2020
pubmed: 16 7 2020
medline: 22 6 2021
Statut: epublish

Résumé

Viral replication is defined by the cellular microenvironment and one key factor is local oxygen tension, where hypoxia inducible factors (HIFs) regulate the cellular response to oxygen. Human immunodeficiency virus (HIV) infected cells within secondary lymphoid tissues exist in a low-oxygen or hypoxic environment in vivo. However, the majority of studies on HIV replication and latency are performed under laboratory conditions where HIFs are inactive. We show a role for HIF-2α in restricting HIV transcription via direct binding to the viral promoter. Hypoxia reduced tumor necrosis factor or histone deacetylase inhibitor, Romidepsin, mediated reactivation of HIV and inhibiting HIF signaling-pathways reversed this phenotype. Our data support a model where the low-oxygen environment of the lymph node may suppress HIV replication and promote latency. We identify a mechanism that may contribute to the limited efficacy of latency reversing agents in reactivating HIV and suggest new strategies to control latent HIV-1.

Identifiants

pubmed: 32665623
doi: 10.1038/s42003-020-1103-1
pii: 10.1038/s42003-020-1103-1
pmc: PMC7360605
doi:

Substances chimiques

Basic Helix-Loop-Helix Transcription Factors 0
endothelial PAS domain-containing protein 1 1B37H0967P
Oxygen S88TT14065

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

376

Subventions

Organisme : Medical Research Council
ID : MR/R022011/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 200838/Z/16/Z
Pays : United Kingdom
Organisme : NIAID NIH HHS
ID : 114266
Pays : United States
Organisme : Medical Research Council
ID : G0801976
Pays : United Kingdom
Organisme : Department of Health
ID : NIHR-RP-2016-06-004
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0400802
Pays : United Kingdom

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Auteurs

Xiaodong Zhuang (X)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Isabela Pedroza-Pacheco (I)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Isabel Nawroth (I)

Institute of Immunity and Immunotherapy, University of Birmingham, Birmingham, B15 2TT, UK.

Anna E Kliszczak (AE)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Andrea Magri (A)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Wayne Paes (W)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Claudia Orbegozo Rubio (CO)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Hongbing Yang (H)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Margaret Ashcroft (M)

Department of Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0AH, UK.

David Mole (D)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Peter Balfe (P)

Institute of Immunity and Immunotherapy, University of Birmingham, Birmingham, B15 2TT, UK.

Persephone Borrow (P)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK.

Jane A McKeating (JA)

Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK. jane.mckeating@ndm.ox.ac.uk.

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