<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yaron JR</submitter><funding>American Heart Association</funding><funding>University of Florida</funding><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | National Institutes of Health</funding><pagination>2371</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7012916</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(1)</volume><pubmed_abstract>Immunopathogenesis in systemic viral infections can induce a septic state with leaky capillary syndrome, disseminated coagulopathy, and high mortality with limited treatment options. Murine gammaherpesvirus-68 (MHV-68) intraperitoneal infection is a gammaherpesvirus model for producing severe vasculitis, colitis and lethal hemorrhagic pneumonia in interferon gamma receptor-deficient (IFNγR&lt;sup>-/-&lt;/sup>) mice. In prior work, treatment with myxomavirus-derived Serp-1 or a derivative peptide S-7 (G&lt;sub>305&lt;/sub>TTASSDTAITLIPR&lt;sub>319&lt;/sub>) induced immune protection, reduced disease severity and improved survival after MHV-68 infection. Here, we investigate the gut bacterial microbiome in MHV-68 infection. Antibiotic suppression markedly accelerated MHV-68 pathology causing pulmonary consoli</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Immune protection is dependent on the gut microbiome in a lethal mouse gammaherpesviral infection.</pubmed_title><pmcid>PMC7012916</pmcid><funding_grant_id>1R01AI100987-01A1</funding_grant_id><funding_grant_id>RC1 HL100202</funding_grant_id><funding_grant_id>00115070</funding_grant_id><funding_grant_id>17GRNT33460327</funding_grant_id><funding_grant_id>R01 AI100987</funding_grant_id><funding_grant_id>1RC1HL100202</funding_grant_id><pubmed_authors>Yaron JR</pubmed_authors><pubmed_authors>Tibbetts SA</pubmed_authors><pubmed_authors>Bullard WL</pubmed_authors><pubmed_authors>Koppang EO</pubmed_authors><pubmed_authors>Munk BH</pubmed_authors><pubmed_authors>Lucas AR</pubmed_authors><pubmed_authors>Keinan S</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Maldonado J</pubmed_authors><pubmed_authors>Ambadapadi S</pubmed_authors><pubmed_authors>Varsani A</pubmed_authors><pubmed_authors>Tafoya AM</pubmed_authors><pubmed_authors>Stern-Harbutte A</pubmed_authors><pubmed_authors>Chavan RN</pubmed_authors><pubmed_authors>Krajmalnik-Brown R</pubmed_authors><pubmed_authors>Lim ES</pubmed_authors><pubmed_authors>Kraberger S</pubmed_authors><pubmed_authors>Kilbourne J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immune protection is dependent on the gut microbiome in a lethal mouse gammaherpesviral infection.</name><description>Immunopathogenesis in systemic viral infections can induce a septic state with leaky capillary syndrome, disseminated coagulopathy, and high mortality with limited treatment options. Murine gammaherpesvirus-68 (MHV-68) intraperitoneal infection is a gammaherpesvirus model for producing severe vasculitis, colitis and lethal hemorrhagic pneumonia in interferon gamma receptor-deficient (IFNγR&lt;sup>-/-&lt;/sup>) mice. In prior work, treatment with myxomavirus-derived Serp-1 or a derivative peptide S-7 (G&lt;sub>305&lt;/sub>TTASSDTAITLIPR&lt;sub>319&lt;/sub>) induced immune protection, reduced disease severity and improved survival after MHV-68 infection. Here, we investigate the gut bacterial microbiome in MHV-68 infection. Antibiotic suppression markedly accelerated MHV-68 pathology causing pulmonary consoli</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Feb</publication><modification>2026-05-02T20:00:39.021Z</modification><creation>2020-05-22T10:40:50Z</creation></dates><accession>S-EPMC7012916</accession><cross_references><pubmed>32047224</pubmed><doi>10.1038/s41598-020-59269-9</doi></cross_references></HashMap>