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Scavenger receptor A (<jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content>) is a phagocytic pattern recognition receptor involved in various cellular processes, including lipid metabolism, recognition, and clearance of pathogens or modified self\u2010molecules. Emerging evidence pointed out that <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content> might act as an immunomodulator that contributes to innate immune defense against invading pathogens. Herein, we examined the role of <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content> in the initiation of type I interferon (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>) response to <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> infection and the virus clearance. Our results showed that <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content>\u2010deficient (<jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content><jats:sup>\u2212\/\u2212<\/jats:sup>) mice were resistant to <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> infection developed by hydrodynamic injection of <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> replicon plasmid. We found lower levels of <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> and viral protein expression in <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content><jats:sup>\u2212\/\u2212<\/jats:sup> mice, which was associated with enhanced type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> production, compared with wild\u2010type controls. Besides, we performed gain and loss of function experiments and determined that <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content> inhibits innate antiviral immune responses to <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content> could interact directly with tumor necrosis factor receptor\u2010associated factor 3 (<jats:styled-content style=\"fixed-case\">TRAF<\/jats:styled-content>3) and inhibit its K63\u2010linked ubiquitination. Moreover, we provided evidence that <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content> negatively regulates the stability of <jats:styled-content style=\"fixed-case\">TRAF<\/jats:styled-content>3 protein by promoting the recruitment of <jats:styled-content style=\"fixed-case\">OTUB<\/jats:styled-content>1 to <jats:styled-content style=\"fixed-case\">TRAF<\/jats:styled-content>3. Our findings indicate that <jats:styled-content style=\"fixed-case\">SRA<\/jats:styled-content> plays a crucial role in innate immune signaling by targeting <jats:styled-content style=\"fixed-case\">TRAF<\/jats:styled-content>3 for degradation and balancing the innate antiviral immunity.<\/jats:p>","DOI":"10.1111\/febs.15035","type":"journal-article","created":{"date-parts":[[2019,8,6]],"date-time":"2019-08-06T18:50:51Z","timestamp":1565117451000},"page":"310-324","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Scavenger receptor A impairs interferon response to <scp>HBV<\/scp> infection by limiting <scp>TRAF<\/scp>3 ubiquitination through recruiting <scp>OTUB<\/scp>1"],"prefix":"10.1111","volume":"287","author":[{"given":"Mengying","family":"Xie","sequence":"first","affiliation":[{"name":"Institute of Molecular Immunology School of Laboratory Medicine and Biotechnology Southern Medical University Guangzhou 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