HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.

Previous studies demonstrate that soluble HIV proteins impact both hepatocyte function and HCV replication in vitro. It has also been reported that HIV can productively infect hepatocytes. We therefore investigated the impact of HIV infection of hepatocytes on HCV expression. The Huh7.5JFH1 cell lin...

Full description

Bibliographic Details
Main Authors: Ling Kong, Jeffrey A Welge, Eleanor A Powell, Jason T Blackard
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3938396?pdf=render
_version_ 1811227480790401024
author Ling Kong
Jeffrey A Welge
Eleanor A Powell
Jason T Blackard
author_facet Ling Kong
Jeffrey A Welge
Eleanor A Powell
Jason T Blackard
author_sort Ling Kong
collection DOAJ
description Previous studies demonstrate that soluble HIV proteins impact both hepatocyte function and HCV replication in vitro. It has also been reported that HIV can productively infect hepatocytes. We therefore investigated the impact of HIV infection of hepatocytes on HCV expression. The Huh7.5JFH1 cell line that constitutively expresses infectious HCV was infected with the lab-adapted strains HIVNL4-3 or HIVYK-JRCSF. HCV expression was quantified via HCV core antigen ELISA, Western blot, and strand-specific real-time PCR for positive-sense and negative-sense HCV RNA. After HIVNL4-3 infection of Huh7.5JFH1 cells, positive-sense and negative-sense HCV RNA levels were elevated compared to HIV uninfected cells. Increased HCV RNA synthesis was also observed after infection of Huh7.5JFH1 cells with HIVYK-JRCSF. HIV-induced HCV core production was decreased in the presence of the anti-HIV drugs AZT, T20, and raltegravir, although these medications had a minimal effect on HCV expression in the absence of HIV. HCV core, NS3, and NS5A protein expression were increased after HIV infection of Huh7.5JFH1 cells. Chemically inactivated HIV had a minimal effect on HCV expression in Huh7.5JFH1 cells suggesting that ongoing viral replication was critical. These data demonstrate that HIV induces HCV RNA synthesis and protein production in vitro and complement previous in vivo reports that HCV RNA levels are elevated in individuals with HIV/HCV co-infection compared to those with HCV mono-infection. These findings suggest that HIV suppression may be a critical factor in controlling liver disease, particularly if the underlying liver disease is not treated.
first_indexed 2024-04-12T09:42:12Z
format Article
id doaj.art-562fe18928974750a598c20bd3e0bf8e
institution Directory Open Access Journal
issn 1932-6203
language English
last_indexed 2024-04-12T09:42:12Z
publishDate 2014-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS ONE
spelling doaj.art-562fe18928974750a598c20bd3e0bf8e2022-12-22T03:38:02ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e8372810.1371/journal.pone.0083728HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.Ling KongJeffrey A WelgeEleanor A PowellJason T BlackardPrevious studies demonstrate that soluble HIV proteins impact both hepatocyte function and HCV replication in vitro. It has also been reported that HIV can productively infect hepatocytes. We therefore investigated the impact of HIV infection of hepatocytes on HCV expression. The Huh7.5JFH1 cell line that constitutively expresses infectious HCV was infected with the lab-adapted strains HIVNL4-3 or HIVYK-JRCSF. HCV expression was quantified via HCV core antigen ELISA, Western blot, and strand-specific real-time PCR for positive-sense and negative-sense HCV RNA. After HIVNL4-3 infection of Huh7.5JFH1 cells, positive-sense and negative-sense HCV RNA levels were elevated compared to HIV uninfected cells. Increased HCV RNA synthesis was also observed after infection of Huh7.5JFH1 cells with HIVYK-JRCSF. HIV-induced HCV core production was decreased in the presence of the anti-HIV drugs AZT, T20, and raltegravir, although these medications had a minimal effect on HCV expression in the absence of HIV. HCV core, NS3, and NS5A protein expression were increased after HIV infection of Huh7.5JFH1 cells. Chemically inactivated HIV had a minimal effect on HCV expression in Huh7.5JFH1 cells suggesting that ongoing viral replication was critical. These data demonstrate that HIV induces HCV RNA synthesis and protein production in vitro and complement previous in vivo reports that HCV RNA levels are elevated in individuals with HIV/HCV co-infection compared to those with HCV mono-infection. These findings suggest that HIV suppression may be a critical factor in controlling liver disease, particularly if the underlying liver disease is not treated.http://europepmc.org/articles/PMC3938396?pdf=render
spellingShingle Ling Kong
Jeffrey A Welge
Eleanor A Powell
Jason T Blackard
HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.
PLoS ONE
title HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.
title_full HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.
title_fullStr HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.
title_full_unstemmed HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.
title_short HIV infection of hepatocytes results in a modest increase in hepatitis C virus expression in vitro.
title_sort hiv infection of hepatocytes results in a modest increase in hepatitis c virus expression in vitro
url http://europepmc.org/articles/PMC3938396?pdf=render
work_keys_str_mv AT lingkong hivinfectionofhepatocytesresultsinamodestincreaseinhepatitiscvirusexpressioninvitro
AT jeffreyawelge hivinfectionofhepatocytesresultsinamodestincreaseinhepatitiscvirusexpressioninvitro
AT eleanorapowell hivinfectionofhepatocytesresultsinamodestincreaseinhepatitiscvirusexpressioninvitro
AT jasontblackard hivinfectionofhepatocytesresultsinamodestincreaseinhepatitiscvirusexpressioninvitro