Format

Send to

Choose Destination
Clin Immunol. 2018 Oct;195:127-138. doi: 10.1016/j.clim.2018.06.001. Epub 2018 Jun 5.

Residual T cell activation and skewed CD8+ T cell memory differentiation despite antiretroviral therapy-induced HIV suppression.

Author information

1
Institute of Infectious Disease and Molecular Medicine and Department of Pathology, Division of Medical Virology, Faculty of Health Sciences, University of Cape Town, South Africa.
2
Institute of Infectious Disease and Molecular Medicine and Department of Pathology, Division of Medical Virology, Faculty of Health Sciences, University of Cape Town, South Africa; Centre for the AIDS Program of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.
3
Centre for the AIDS Program of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa.
4
Centre for the AIDS Program of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, United States.
5
Institute of Infectious Disease and Molecular Medicine and Department of Pathology, Division of Medical Virology, Faculty of Health Sciences, University of Cape Town, South Africa. Electronic address: wendy.burgers@uct.ac.za.

Abstract

HIV infection results in excessive T cell activation and dysfunction which may persist even during effective antiretroviral therapy (ART). The dynamics of immune 'deactivation' and extent to which T cell memory subsets normalize after ART are unclear. We longitudinally assessed the influence of 1 year of ART on the phenotype of T cells in HIV-infected African women, relative to matched HIV-uninfected women, using activation (CD38, HLA-DR) and differentiation markers (CD27, CD45RO). ART induced a substantial reduction in T cell activation, but remained higher than HIV-uninfected controls. ART largely normalized the distribution of CD4+ T cell memory subsets, while the distribution of CD8+ T cell memory subsets remained significantly skewed compared to HIV-uninfected individuals. Thus, there was a considerable but only partial reversal of T cell defects upon ART. Understanding T cell impairment may provide important insights into mechanisms of HIV pathogenesis in the era of ART.

KEYWORDS:

Antiretroviral therapy; Chronic HIV; T cell activation; T cell differentiation

PMID:
29883708
DOI:
10.1016/j.clim.2018.06.001

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center