<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>57(3)</volume><submitter>Wang J</submitter><pubmed_abstract>The persistent global burden of hepatitis B virus (HBV) infection has prompted ongoing investigations into host determinants of viral control. In this study, we investigate the regulatory influence of the host gene cleavage stimulation factor subunit 2 (CSTF2) on HBV replication dynamics. We demonstrate differential CSTF2 expression across the spectrum of HBV infection phases, with upregulated expression noted during the immune-reactive and inactive carrier states compared with the immune-tolerant phase. Notably, dose-responsive attenuation of HBV DNA, as well as surface and core protein levels, is observed subsequent to CSTF2 overexpression, whereas HBV RNA levels remain unaffected. Upon HBV transfection, a notable alteration in CSTF2 subcellular localization is discerned, suggesting acti</pubmed_abstract><journal>Acta biochimica et biophysica Sinica</journal><pagination>486-496</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11986456</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The host gene &amp;lt;i&amp;gt;CSTF2&amp;lt;/i&amp;gt; regulates HBV replication via HBV PRE-induced nuclear export.</pubmed_title><pmcid>PMC11986456</pmcid><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Xie W</pubmed_authors><pubmed_authors>Lu M</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Shen Z</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Mao R</pubmed_authors><pubmed_authors>Wang J</pubmed_authors></additional><is_claimable>false</is_claimable><name>The host gene &amp;lt;i&amp;gt;CSTF2&amp;lt;/i&amp;gt; regulates HBV replication via HBV PRE-induced nuclear export.</name><description>The persistent global burden of hepatitis B virus (HBV) infection has prompted ongoing investigations into host determinants of viral control. In this study, we investigate the regulatory influence of the host gene cleavage stimulation factor subunit 2 (CSTF2) on HBV replication dynamics. We demonstrate differential CSTF2 expression across the spectrum of HBV infection phases, with upregulated expression noted during the immune-reactive and inactive carrier states compared with the immune-tolerant phase. Notably, dose-responsive attenuation of HBV DNA, as well as surface and core protein levels, is observed subsequent to CSTF2 overexpression, whereas HBV RNA levels remain unaffected. Upon HBV transfection, a notable alteration in CSTF2 subcellular localization is discerned, suggesting acti</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-06-01T20:14:31.035Z</modification><creation>2025-07-03T03:04:41.656Z</creation></dates><accession>S-EPMC11986456</accession><cross_references><pubmed>39722572</pubmed><doi>10.3724/abbs.2024216</doi></cross_references></HashMap>