Limited HIV-2 reservoirs in central-memory CD4 T-cells associated to CXCR6 co-receptor expression in attenuated HIV-2 infection.


Journal

PLoS pathogens
ISSN: 1553-7374
Titre abrégé: PLoS Pathog
Pays: United States
ID NLM: 101238921

Informations de publication

Date de publication:
05 2019
Historique:
received: 15 11 2018
accepted: 10 04 2019
revised: 29 05 2019
pubmed: 17 5 2019
medline: 19 11 2019
entrez: 17 5 2019
Statut: epublish

Résumé

The low pathogenicity and replicative potential of HIV-2 are still poorly understood. We investigated whether HIV-2 reservoirs might follow the peculiar distribution reported in models of attenuated HIV-1/SIV infections, i.e. limited infection of central-memory CD4 T lymphocytes (TCM). Antiretroviral-naive HIV-2 infected individuals from the ANRS-CO5 (12 non-progressors, 2 progressors) were prospectively included. Peripheral blood mononuclear cells (PBMCs) were sorted into monocytes and resting CD4 T-cell subsets (naive [TN], central- [TCM], transitional- [TTM] and effector-memory [TEM]). Reactivation of HIV-2 was tested in 30-day cultures of CD8-depleted PBMCs. HIV-2 DNA was quantified by real-time PCR. Cell surface markers, co-receptors and restriction factors were analyzed by flow-cytometry and multiplex transcriptomic study. HIV-2 DNA was undetectable in monocytes from all individuals and was quantifiable in TTM from 4 individuals (median: 2.25 log10 copies/106 cells [IQR: 1.99-2.94]) but in TCM from only 1 individual (1.75 log10 copies/106 cells). HIV-2 DNA levels in PBMCs (median: 1.94 log10 copies/106 PBMC [IQR = 1.53-2.13]) positively correlated with those in TTM (r = 0.66, p = 0.01) but not TCM. HIV-2 reactivation was observed in the cells from only 3 individuals. The CCR5 co-receptor was distributed similarly in cell populations from individuals and donors. TCM had a lower expression of CXCR6 transcripts (p = 0.002) than TTM confirmed by FACS analysis, and a higher expression of TRIM5 transcripts (p = 0.004). Thus the low HIV-2 reservoirs differ from HIV-1 reservoirs by the lack of monocytic infection and a limited infection of TCM associated to a lower expression of a potential alternative HIV-2 co-receptor, CXCR6 and a higher expression of a restriction factor, TRIM5. These findings shed new light on the low pathogenicity of HIV-2 infection suggesting mechanisms close to those reported in other models of attenuated HIV/SIV infection models.

Identifiants

pubmed: 31095640
doi: 10.1371/journal.ppat.1007758
pii: PPATHOGENS-D-18-02196
pmc: PMC6541300
doi:

Substances chimiques

Antiviral Restriction Factors 0
CXCR6 protein, human 0
Carrier Proteins 0
Receptors, CXCR6 0
Tripartite Motif Proteins 0
TRIM5 protein, human EC 2.3.2.27
Ubiquitin-Protein Ligases EC 2.3.2.27

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1007758

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Assia Samri (A)

Sorbonne Université, Inserm 1135, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.

Charlotte Charpentier (C)

IAME, UMR 1137, Inserm, Université Paris Diderot, Sorbonne Paris Cité, Laboratoire de Virologie, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France.

Mariama Sadjo Diallo (MS)

Sorbonne Université, Inserm 1135, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.

Mélanie Bertine (M)

IAME, UMR 1137, Inserm, Université Paris Diderot, Sorbonne Paris Cité, Laboratoire de Virologie, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France.

Sophie Even (S)

Sorbonne Université, Inserm 1135, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.

Véronique Morin (V)

Sorbonne-Université, Inserm 1135, CNRS ERL8255, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.

Anne Oudin (A)

Sorbonne-Université, Inserm 1135, CNRS ERL8255, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.

Christophe Parizot (C)

Sorbonne Université, Inserm 1135, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.
Assistance Publique-Hôpitaux de Paris, Groupement Hospitalier Pitié-Salpêtrière, Département d'Immunologie, Paris, France.

Gilles Collin (G)

IAME, UMR 1137, Inserm, Université Paris Diderot, Sorbonne Paris Cité, Laboratoire de Virologie, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France.

Anne Hosmalin (A)

Institut Cochin, Inserm, U1016, CNRS, UMR8104, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.

Rémi Cheynier (R)

Institut Cochin, Inserm, U1016, CNRS, UMR8104, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.

Rodolphe Thiébaut (R)

Inserm U1219 Bordeaux Population Health, INRIA SISTM, Univ. Bordeaux, Bordeaux, France.

Sophie Matheron (S)

Inserm, IAME, UMR 1137, Univ. Paris Diderot, Sorbonne Paris Cité, Assistance Publique -Hôpitaux de Paris, Service des Maladies Infectieuses et Tropicales, Hôpital Bichat, HUPNVS, Paris, France.

Fideline Collin (F)

Inserm U1219 Bordeaux Population Health, INRIA SISTM, Univ. Bordeaux, Bordeaux, France.

Rima Zoorob (R)

Sorbonne-Université, Inserm 1135, CNRS ERL8255, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, Paris, France.

Françoise Brun-Vézinet (F)

University Paris7, Denis Diderot, Paris, France.

Brigitte Autran (B)

Sorbonne Université, Inserm 1135, Centre d'immunologie et des maladies infectieuses, Cimi-Paris, AP-HP, Hôpital universitaire Pitié-Salpêtrière, Paris, France.

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