<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hetta HF</submitter><funding>NIDDK NIH HHS</funding><pagination>703-712</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5756491</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>65(8)</volume><pubmed_abstract>Extra-hepatic compartments might contribute to hepatitis C virus (HCV) persistence and extra-hepatic manifestations. Therefore, we investigated HCV infection in colonic tissue in patients with chronic hepatitis C (CHC) and its relationship with HCV pathogenesis. Colonic biopsies were collected from three groups with CHC infection: treatment naïve (TN; n=12), non-responders (NR; n=10) to anti-HCV therapy (pegylated interferon-α and ribavirin) and sustained virologic response (SVR; n=10) and from a fourth healthy control group (n=10). Liver biopsies were examined to assess inflammation and fibrosis. HCV infection and colonic T regulatory (Treg) frequency were detected by immunohistochemistry. HCV core and NS3 proteins were detected in B cells and macrophage/monocytes of 42 % and 25 % of TN and 50 % and 30 % of NR, respectively, but not in SVR or control group. The numbers of cells expressing HCV proteins were positively correlated with both HCV viral load and colonic Treg frequency. A significant negative correlation between HCV-expressing cells with both liver inflammation and fibrosis was identified. Our study provides evidence that HCV can infect B cells and macrophages of the colon. The correlations between HCV infection in colonic tissue and HCV viral load and liver pathology underline the significance of this extra-hepatic infection in HCV pathogenesis and response to therapy.</pubmed_abstract><journal>Journal of medical microbiology</journal><pubmed_title>Extra-hepatic infection of hepatitis C virus in the colon tissue and its relationship with hepatitis C virus pathogenesis.</pubmed_title><pmcid>PMC5756491</pmcid><funding_grant_id>K24 DK070528</funding_grant_id><funding_grant_id>P30 DK078392</funding_grant_id><pubmed_authors>Shata MTM</pubmed_authors><pubmed_authors>Hetta HF</pubmed_authors><pubmed_authors>Ahmed SH</pubmed_authors><pubmed_authors>Sherman KE</pubmed_authors><pubmed_authors>Mekky MA</pubmed_authors><pubmed_authors>Khalil NK</pubmed_authors><pubmed_authors>Daef EA</pubmed_authors><pubmed_authors>Nassar MI</pubmed_authors><pubmed_authors>El-Feky MA</pubmed_authors><pubmed_authors>Medhat A</pubmed_authors><pubmed_authors>Mohamed WA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Extra-hepatic infection of hepatitis C virus in the colon tissue and its relationship with hepatitis C virus pathogenesis.</name><description>Extra-hepatic compartments might contribute to hepatitis C virus (HCV) persistence and extra-hepatic manifestations. Therefore, we investigated HCV infection in colonic tissue in patients with chronic hepatitis C (CHC) and its relationship with HCV pathogenesis. Colonic biopsies were collected from three groups with CHC infection: treatment naïve (TN; n=12), non-responders (NR; n=10) to anti-HCV therapy (pegylated interferon-α and ribavirin) and sustained virologic response (SVR; n=10) and from a fourth healthy control group (n=10). Liver biopsies were examined to assess inflammation and fibrosis. HCV infection and colonic T regulatory (Treg) frequency were detected by immunohistochemistry. HCV core and NS3 proteins were detected in B cells and macrophage/monocytes of 42 % and 25 % of TN and 50 % and 30 % of NR, respectively, but not in SVR or control group. The numbers of cells expressing HCV proteins were positively correlated with both HCV viral load and colonic Treg frequency. A significant negative correlation between HCV-expressing cells with both liver inflammation and fibrosis was identified. Our study provides evidence that HCV can infect B cells and macrophages of the colon. The correlations between HCV infection in colonic tissue and HCV viral load and liver pathology underline the significance of this extra-hepatic infection in HCV pathogenesis and response to therapy.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Aug</publication><modification>2024-11-15T22:05:57.186Z</modification><creation>2019-03-27T00:14:38Z</creation></dates><accession>S-EPMC5756491</accession><cross_references><pubmed>27166142</pubmed><doi>10.1099/jmm.0.000272</doi></cross_references></HashMap>