Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

HIV-Infected Hepatic Stellate Cells or HCV-Infected Hepatocytes Are Unable to Promote Latency Reversal among HIV-Infected Mononuclear Cells

Cinthya Alicia Marcela López
ORCID logo ,
Rosa Nicole Freiberger
ORCID logo ,
Franco Agustin Sviercz
,
Jorge Quarleri
* ORCID logo ,
María Victoria Delpino
* ORCID logo
Version 1 : Received: 20 December 2023 / Approved: 21 December 2023 / Online: 21 December 2023 (07:03:44 CET)

A peer-reviewed article of this Preprint also exists.

López, C.A.M.; Freiberger, R.N.; Sviercz, F.A.; Quarleri, J.; Delpino, M.V. HIV-Infected Hepatic Stellate Cells or HCV-Infected Hepatocytes Are Unable to Promote Latency Reversal among HIV-Infected Mononuclear Cells. Pathogens 2024, 13, 134. López, C.A.M.; Freiberger, R.N.; Sviercz, F.A.; Quarleri, J.; Delpino, M.V. HIV-Infected Hepatic Stellate Cells or HCV-Infected Hepatocytes Are Unable to Promote Latency Reversal among HIV-Infected Mononuclear Cells. Pathogens 2024, 13, 134.

Abstract

Due to a common mode of transmission through infected human blood, hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection is relatively prevalent. In alignment with this, HCV co-infection is associated with an increased size of the HIV reservoir in highly active antiretroviral therapy (HAART)-treated individuals. Hence, it is crucial to comprehend the physiological mechanisms governing the latency and reactivation of HIV in reservoirs. Consequently, our study delves into the interplay between HCV/HIV coinfection in liver cells and its impact on the modulation of HIV latency. We utilized the latently infected monocytic cell line (U1) and the latently infected T cell line (J-Lat) and found that mediators produced by the infection of hepatic stellate cells and hepatocytes with HIV and HCV, respectively, were incapable of inducing latency reversal under the studied conditions. This may favor the maintenance of the HIV reservoir size among latently infected mononuclear cells in the liver. Further investigations are essential to elucidate the role of the interaction between liver cells in regulating HIV latency and/or reactivation, providing a physiologically relevant model for comprehending reservoir microenvironments in vivo.

Keywords

HIV; HCV; coinfection; J-Lat; U1; latency reversal; liver

Subject

Biology and Life Sciences, Immunology and Microbiology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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