Difference in Markers of Microbial Translocation and Cell Apoptosis in HIV Monoinfected and HIV/HCV Coinfected Patients

Abstract

Immune activation in human immunodeficiency virus (HIV) infection is driven by microbial translocation and in HIV patients is one of the contributors to faster progression of liver disease along with increased cell apoptosis. The aim of the study was to compare microbial translocation and apoptosis markers in HIV monoinfected and HIV/hepatitis C virus (HCV) coinfected patients, depending on HIV immune status and antiretroviral treatment (ART). We analysed data for 78 HIV monoinfected and 105 HIV/HCV coinfected patients from the Rīga East University Hospital. Lipopolysaccharide (LPS), endotoxin core antibodies (EndoCAb), cytokeratin 18 (CK18) and cyto-chrome c (Cyt-c) levels were measured. No significant difference in LPS, EndoCAb, Cyt-c levels between HIV and HIV/HCV patients was found. The CK18 level was higher in the HIV/HCV group. Correlation between CD4+ cell count and EndoCAb antibodies was found in HCV positive patients. There was a significant effect of ART on markers for EndoCAb IgA and EndoCAb IgM antibodies in the HIV monoinfected group. Correlation between CD4+ cell count and EndoCAb antibodies and LPS was found in HIV/HCV patients on ART. Coinfection with HCV can lead to more pronounced response in EndoCAb antibody production and higher levels of cell apoptosis markers, despite similar LPS levels. ART has a positive effect on immune activation.

The Level of Cytokeratin 18 in Patients with HIV and Viral Hepatitis C Co-Infection in Latvia

“…At the same time, there was no association between CK18 and other markers of liver fibrosis in this group. Higher levels of CK18 in HIV/HCV patients than in HIV mono-infected patients have been shown previously in two studies in Latvian cohorts (Vîksna et al, 2019;Madelâne et al, 2019). Our study merges data from both Latvian studies and provides CK18 levels in a relatively large group of HIV/HCV coinfected and HIV mono-infected patients, and the association of CK18 levels with other non-invasive markers of liver fibrosis, and describes CK18 dynamics in a fourmonth-long period.…”