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T-cell and B-cell perturbations are similar in ART-naive HIV-1 and HIV-1/2 dually infected patients

Hønge, Bo L.a,b; Petersen, Mikkel S.b; Jespersen, Sannea,c; Medina, Candidad; Té, David D.S.d; Kjerulff, Bertramb; Jensen, Mads M.a,b; Steiniche, Dittea,c; Esbjörnsson, Joakime,f; Laursen, Alex L.c; Wejse, Christiana,c,g; Krarup, Henrikh; Møller, Bjarne K.b; Erikstrup, Christianb for the Bissau HIV Cohort study group

doi: 10.1097/QAD.0000000000002185
BASIC SCIENCE
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Background: HIV-2 may slow progression of a subsequently acquired HIV-1 infection through cross-neutralizing antibodies and polyfunctional CD8+ T cells. We hypothesized that HIV-1/2 dually infected patients compared with HIV-1-infected patients had more preserved immune maturation subsets and less immune activation of T and B cells.

Methods: ART-naive patients with HIV-1 (n = 83) or HIV-1/2 dual (n = 27) infections were included in this cross-sectional study at an HIV clinic in Guinea-Bissau. Peripheral blood mononuclear cells (PBMCs) were analyzed by flow cytometry according to T-cell maturation and activation, regulatory T-cell fraction, and B-cell maturation and activation.

Results: HIV-1/2 dually infected patients had lower levels of HIV-1 RNA compared with patients with HIV-1 infection, but the levels of total HIV RNA (HIV-1 and HIV-2) were similar in the two patient groups. T-cell maturation, and proportions of regulatory T cells (FoxP3+) were also similar in the two groups. HIV-1/2 dually infected patients had higher proportions of CD4+ and CD8+ T cells positive for the activation marker CD38, but there was no difference in other T-cell activation markers (CD28, CTLA-4, PD-1). HIV-1/2 dually infected patients also had higher proportions of IgM-only B cells and plasmablasts.

Conclusion: HIV-1/2 was not associated with less immune perturbations than for HIV-1 infection.

aBandim Health Project, Indepth Network, Bissau, Guinea-Bissau

bDepartment of Clinical Immunology

cDepartment of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark

dNational HIV Programme, Ministry of Health, Bissau, Guinea-Bissau

eDepartment of Laboratory Medicine, Lund University, Lund, Sweden

fNuffield Department of Medicine, University of Oxford, Oxford, United Kingdom

gGloHAU, Center for Global Health, School of Public Health, Aarhus University, Aarhus

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

Correspondence to Bo L. Hønge, Department of Clinical Immunology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus, Denmark. Tel: +45 23718870; fax: +45 78455015; e-mail: bohonge@gmail.com

Received 31 July, 2018

Revised 1 February, 2019

Accepted 5 February, 2019

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