T-cell and B-cell perturbations identify distinct differences in HIV-2 compared with HIV-1-induced immunodeficiency.


Journal

AIDS (London, England)
ISSN: 1473-5571
Titre abrégé: AIDS
Pays: England
ID NLM: 8710219

Informations de publication

Date de publication:
01 06 2019
Historique:
pubmed: 8 3 2019
medline: 22 7 2020
entrez: 8 3 2019
Statut: ppublish

Résumé

For unknown reasons, HIV-2 is less pathogenic than HIV-1, and HIV-2-induced immunodeficiency may be different from that caused by HIV-1. Previous immunological studies have hinted at possible shifts in both T-cell and B-cell subsets, which we aimed to characterize further. From an HIV clinic in Guinea-Bissau, 63 HIV-2, 83 HIV-1, and 26 HIV-negative participants were included. All HIV-infected participants were ART-naive. The following cell subsets were analysed by flow cytometry; T cells (maturation and activation), regulatory T cells, and B cells (maturation and activation). After standardizing for sex, age, and CD4 T-cell count HIV-2 had 0.938 log10 copies/ml lower HIV RNA levels than the HIV-1-infected patients. Whereas T-cell maturation and regulatory T-cell profiles were similar between patients, HIV-2-infected patients had higher proportions of CD8CD28 and lower proportions of CD8PD-1+ T cells than HIV-1-infected patients. This finding was independent of HIV RNA levels. HIV-2 was also associated with a more preserved proportion of naive B cells. HIV-2 is characterized by lower viral load, and lower T-cell activation, which may account for the slower disease progression.

Sections du résumé

BACKGROUND
For unknown reasons, HIV-2 is less pathogenic than HIV-1, and HIV-2-induced immunodeficiency may be different from that caused by HIV-1. Previous immunological studies have hinted at possible shifts in both T-cell and B-cell subsets, which we aimed to characterize further.
METHODS
From an HIV clinic in Guinea-Bissau, 63 HIV-2, 83 HIV-1, and 26 HIV-negative participants were included. All HIV-infected participants were ART-naive. The following cell subsets were analysed by flow cytometry; T cells (maturation and activation), regulatory T cells, and B cells (maturation and activation).
RESULTS
After standardizing for sex, age, and CD4 T-cell count HIV-2 had 0.938 log10 copies/ml lower HIV RNA levels than the HIV-1-infected patients. Whereas T-cell maturation and regulatory T-cell profiles were similar between patients, HIV-2-infected patients had higher proportions of CD8CD28 and lower proportions of CD8PD-1+ T cells than HIV-1-infected patients. This finding was independent of HIV RNA levels. HIV-2 was also associated with a more preserved proportion of naive B cells.
CONCLUSION
HIV-2 is characterized by lower viral load, and lower T-cell activation, which may account for the slower disease progression.

Identifiants

pubmed: 30845070
doi: 10.1097/QAD.0000000000002184
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1131-1141

Auteurs

Bo L Hønge (BL)

Bandim Health Project, Indepth Network, Bissau, Guinea-Bissau.
Department of Clinical Immunology.

Mikkel S Petersen (MS)

Department of Clinical Immunology.

Sanne Jespersen (S)

Bandim Health Project, Indepth Network, Bissau, Guinea-Bissau.
Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark.

Candida Medina (C)

National HIV Programme, Ministry of Health.

David D S Té (DDS)

National HIV Programme, Ministry of Health.

Bertram Kjerulff (B)

Department of Clinical Immunology.

Thomas Engell-Sørensen (T)

Bandim Health Project, Indepth Network, Bissau, Guinea-Bissau.
Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark.

Tina Madsen (T)

Bandim Health Project, Indepth Network, Bissau, Guinea-Bissau.
Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark.

Alex L Laursen (AL)

Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark.

Christian Wejse (C)

Bandim Health Project, Indepth Network, Bissau, Guinea-Bissau.
Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark.
GloHAU, Center for Global Health, School of Public Health, Aarhus University.

Henrik Krarup (H)

Section of Molecular Diagnostics, Clinical Biochemistry, Aalborg University Hospital, Denmark.

Bjarne K Møller (BK)

Department of Clinical Immunology.

Christian Erikstrup (C)

Department of Clinical Immunology.

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