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. 2021 Oct 14;13(10):2074. doi: 10.3390/v13102074

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Graphical summary of this study. Hepatitis C virus infection in the liver of HIV infected patients stimulates the production of chemokines including CCL5 (RANTES), IP-10 (CXL10), which induces migration of CCR5+CXCR3+ T cells from the peripheral blood to the liver. These CCR5+CXCR3+ T cells infiltrating into the liver are chronically activated, terminally differentiated and have an exhausted phenotype. Upon HCV peptide stimulation, these cells secrete more pro-fibrogenic cytokine (TGF-β) rather than antiviral cytokines (IFN-γ and IL-2), which may favor a profibrogenic intrahepatic microenvironment in HIV/HCV coinfection, causing advanced liver disease.