Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Feb;17(2):89-105.
doi: 10.1111/hiv.12310. Epub 2015 Oct 10.

Immune activation in the course of HIV-1 infection: Causes, phenotypes and persistence under therapy

M Younas  1 , C Psomas  2   3 , J Reynes  2   3   4 , P Corbeau  1   4   5
Affiliations
Free article
Review

Immune activation in the course of HIV-1 infection: Causes, phenotypes and persistence under therapy

M Younas et al. HIV Med. 2016 Feb.
Free article

Abstract

Systemic immune activation is a striking consequence of HIV-1 infection. Even in virologically suppressed patients, some hyperactivity of the immune system and even of the endothelium and of the coagulation pathway may persist. Apart from immune deficiency, this chronic activation may contribute to various morbidities including atherothrombosis, neurocognitive disorders, liver steatosis and osteoporosis, which are currently main challenges. It is therefore of major importance to better understand the causes and the phenotypes of immune activation in the course of HIV-1 infection. In this review we will discuss the various causes of immune activation in HIV-1 infected organisms: the presence of the virus together with other microbes, eventually coming from the gut, CD4+ T cell lymphopenia, senescence and dysregulation of the immune system, and/or genetic factors. We will also describe the activation of the immune system: CD4+ and CD8+ T cells, B cells, NKT and NK cells, dendritic cells, monocytes and macrophages, and neutrophils of the inflammation cascade, as well as of the endothelium and the coagulation system. Finally, we will see that antiretroviral therapy reduces the hyperactivity of the immune and coagulation systems and the endothelial dysfunction, but often does not abolish it. A better knowledge of this phenomenon might help us to identify biomarkers predictive of non AIDS-linked comorbidities, and to define new strategies aiming at preventing their emergence.

Keywords: antiretroviral therapy; cell activation; coagulation; endothelium; inflammation; microbial translocation.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles