<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Zhang F</submitter><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><pubmed_abstract>&lt;h4>Background and aims&lt;/h4>Hepatitis B virus (HBV) and hepatitis C virus (HCV) share transmission routes and often coinfect the liver, leading to accelerated liver disease progression. In the era of direct-acting antivirals (DAAs) for HCV, the clinical impact of coinfection is further complicated by reports of HBV reactivation following HCV cure. While HCV-induced interferon (IFN) responses are known to suppress HBV, the underlying mechanisms remain incompletely understood. This study aimed to investigate how HCV modulates HBV infection in the setting of coinfection and to identify strategies to prevent HBV reactivation post-HCV clearance.&lt;h4>Approach and results&lt;/h4>We utilized a multicellular liver culture model composed of human-induced pluripotent stem cell (hiPSC)-derived hepatocytes</pubmed_abstract><journal>Hepatology (Baltimore, Md.)</journal><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12869898</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL1β signaling mediates the interaction between hepatitis B and C viruses.</pubmed_title><pmcid>PMC12869898</pmcid><funding_grant_id>R00 AI141742</funding_grant_id><funding_grant_id>DP2 AI170515</funding_grant_id><funding_grant_id>R01 DK125100</funding_grant_id><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Kwong AC</pubmed_authors><pubmed_authors>Feng Z</pubmed_authors><pubmed_authors>Ha EH</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Bian L</pubmed_authors><pubmed_authors>Ning L</pubmed_authors><pubmed_authors>Dao Thi VL</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Sanchez E</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Foo SS</pubmed_authors><pubmed_authors>O'Shaughnessy K</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Chen S</pubmed_authors><pubmed_authors>Yu Y</pubmed_authors><pubmed_authors>Wu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL1β signaling mediates the interaction between hepatitis B and C viruses.</name><description>&lt;h4>Background and aims&lt;/h4>Hepatitis B virus (HBV) and hepatitis C virus (HCV) share transmission routes and often coinfect the liver, leading to accelerated liver disease progression. In the era of direct-acting antivirals (DAAs) for HCV, the clinical impact of coinfection is further complicated by reports of HBV reactivation following HCV cure. While HCV-induced interferon (IFN) responses are known to suppress HBV, the underlying mechanisms remain incompletely understood. This study aimed to investigate how HCV modulates HBV infection in the setting of coinfection and to identify strategies to prevent HBV reactivation post-HCV clearance.&lt;h4>Approach and results&lt;/h4>We utilized a multicellular liver culture model composed of human-induced pluripotent stem cell (hiPSC)-derived hepatocytes</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-07-15T06:12:25.89Z</modification><creation>2026-06-30T03:21:37.394Z</creation></dates><accession>S-EPMC12869898</accession><cross_references><pubmed>40938198</pubmed><doi>10.1097/hep.0000000000001525</doi><doi>10.1097/HEP.0000000000001525</doi></cross_references></HashMap>