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HCV coinfection contributes to HIV pathogenesis by increasing immune exhaustion in CD8 T-cells.

HCV coinfection contributes to HIV pathogenesis by increasing immune exhaustion in CD8 T-cells.
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Rallón N, García M, García-Samaniego J, Rodríguez N, Cabello A, Restrepo C, Álvarez B, García R, Górgolas M, Benito JM,


Rallón N, García M, García-Samaniego J, Rodríguez N, Cabello A, Restrepo C, Álvarez B, García R, Górgolas M, Benito JM, (click to view)

Rallón N, García M, García-Samaniego J, Rodríguez N, Cabello A, Restrepo C, Álvarez B, García R, Górgolas M, Benito JM,

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PloS one 2017 03 2112(3) e0173943 doi 10.1371/journal.pone.0173943

Abstract
BACKGROUND
There are several contributors to HIV-pathogenesis or insufficient control of the infection. However, whether HIV/HCV-coinfected population exhibits worst evolution of HIV-pathogenesis remains unclear. Recently, some markers of immune exhaustion have been proposed as preferentially upregulated on T-cells during HIV-infection. Herein, we have analyzed T-cell exhaustion together with several other contributors to HIV-pathogenesis that could be affected by HCV-coinfection.

PATIENTS AND METHODS
Ninety-six patients with chronic HIV-infection (60 HIV-monoinfected and 36 HIV/HCV-coinfected), and 20 healthy controls were included in the study. All patients were untreated for both infections. Several CD4 and CD8 T-cell subsets involved in HIV-pathogenesis were investigated. Non-parametric tests were used to establish differences between groups and associations between variables. Multivariate linear regression was used to ascertain the variables independently associated with CD4 counts.

RESULTS
HIV-patients presented significant differences compared to healthy controls in most of the parameters analyzed. Both HIV and HIV/HCV groups were comparable in terms of age, CD4 counts and HIV-viremia. Compared to HIV group, HIV/HCV group presented significantly higher levels of exhaustion (Tim3+PD1- subset) in total CD8+ T-cells (p = 0.003), and higher levels of exhaustion in CD8+HLADR+CD38+ (p = 0.04), CD8+HLADR-CD38+ (p = 0.009) and CD8+HLADR-CD38- (p = 0.006) subsets of CD8+ T-cells. Interestingly these differences were maintained after adjusting by CD4 counts and HIV-viremia.

CONCLUSIONS
We show a significant impact of HCV-coinfection on CD8 T-cells exhaustion, an important parameter associated with CD8 T-cell dysfunction in the setting of chronic HIV-infection. The relevance of this phenomenon on immunological and/or clinical HIV progression prompts HCV treatment to improve management of coinfected patients.

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