Publication

Back to overview

The Interplay Between Host Genetic Variation, Viral Replication, and Microbial Translocation in Untreated HIV-Infected Individuals.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Perkins Molly R, Bartha Istvan, Timmer J Katherina, Liebner Julia C, Wolinsky David, Wollinsky David, Günthard Huldrych F, Hauser Christoph, Bernasconi Enos, Hoffmann Matthias, Calmy Alexandra, Battegay Manuel, Telenti Amalio, Douek Daniel C, Fellay Jacques, Swiss HIV Cohort Study,
Project Swiss HIV Cohort Study (SHCS)
Show all

Original article (peer-reviewed)

Journal The Journal of infectious diseases
Volume (Issue) 212(4)
Page(s) 578 - 84
Title of proceedings The Journal of infectious diseases
DOI 10.1093/infdis/jiv089

Open Access

URL http://doi.org/10.1093/infdis/jiv089
Type of Open Access Publisher (Gold Open Access)

Abstract

Systemic immune activation, a major determinant of human immunodeficiency virus (HIV) disease progression, is the result of a complex interplay between viral replication, dysregulation of the immune system, and microbial translocation due to gut mucosal damage. Although human genetic variants influencing HIV load have been identified, it is unknown how much the host genetic background contributes to interindividual differences in other determinants of HIV pathogenesis such as gut damage and microbial translocation. Using samples and data from 717 untreated participants in the Swiss HIV Cohort Study and a genome-wide association study design, we searched for human genetic determinants of plasma levels of intestinal fatty acid-binding protein (I-FABP/FABP2), a marker of gut damage, and of soluble CD14 (sCD14), a marker of lipopolysaccharide bioactivity and microbial translocation. We also assessed the correlations between HIV load, sCD14, and I-FABP. Although we found no genome-wide significant determinant of the tested plasma markers, we observed strong associations between sCD14 and both HIV load and I-FABP, shedding new light on the relationships between processes that drive progression of untreated HIV infection.
-