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Original article

HIV infection rather than concurrent opportunistic infections drives most systemic procoagulant, vascular and damage responses – a prospective cohort study in central Africa

Saskia Janssen, Michaela AM Huson, Kara K Osbak, Elie-Gide Rossatanga, Abraham Alabi, René Lutter, Martin P Grobusch, Tom van der Poll

Corresponding author name: Saskia Janssen
Corresponding author e-mail: s.janssen@amc.uva.nl

Citation: Antiviral Therapy 2017; 22:153-161
doi: 10.3851/IMP3100

Date accepted: 16 September 2016
Date published online: 05 January 2017

Abstract

Background: HIV infection is accompanied by various systemic host responses, including activation of coagulation and the vascular endothelium. We sought to determine the impact of opportunistic coinfections in a central African setting.

Methods: This prospective study included 98 HIV-infected individuals in Gabon initiating combination antiretroviral therapy (cART) and followed them up for 6 months. Patients were stratified according to the presence of active tuberculosis (TB; n=19), mucocutaneous opportunistic infection (n=9) or no opportunistic infection (n=70). HIV-uninfected subjects were included as controls (n=32). Plasma concentrations of 14 markers of coagulation, endothelial activation, extracellular matrix formation and tissue damage were measured with a multiplex assay at baseline and months 3 and 6 after cART initiation.

Results: HIV-infected patients showed elevated plasma levels of all biomarkers measured with exception of protein C, which was reduced. Concurrent TB was only associated with elevated concentrations of D-dimer, metallopeptidase inhibitor 1 and Tenascin-C. Mucocutaneous coinfection did not alter HIV-associated responses. Most markers measured declined but remained elevated despite response to cART.

Conclusions: HIV infection is associated with systemic pro-coagulant, vascular and damage responses. In an ambulatory setting, concurrent opportunistic infections have little if any influence on these responses and normalization is incomplete after response to cART. This suggests that these responses are mainly driven by HIV-associated immune activation and less so by opportunistic infections.

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