<?xml version="1.0" encoding="UTF-8"?>

<?xml-stylesheet type="text/xsl" href="/static/oaitohtml.xsl"?>

<!--
<?xml-stylesheet type="text/xsl" href="/oaitohtml.xsl"?>
-->

<OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
    <responseDate>2026-10-11T21:47:04Z</responseDate>
    <request verb="GetRecord" metadataPrefix="oai_dc" identifier="10.57760/sciencedb.41644" >https://www.scidb.cn/oai</request>
<GetRecord>
    <record>
    <header >
    <identifier>10.57760/sciencedb.41644</identifier>
    <datestamp>2026-07-09T09:56:33Z</datestamp>
</header>
    <metadata>
        
<oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:date>2026-07-09</dc:date>
  <dc:title>A gut commensal bacterium enhances orthoflavivirus E protein thermostability to enable fecal-oral transmission</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.41644</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Orthoflaviviruses&amp;nbsp;are typically maintained in nature through mosquito borne cycles. How some strains acquire the ability to transmit via direct, non vector routes in vertebrate hosts remains a key evolutionary question. Here, using Tembusu virus (TMUV) in an avian model, we identify a molecular mechanism that explains its cross species transmission from mosquitoes to avian populations. We demonstrate that avian hosts are highly susceptible to TMUV via the oral (intragastric) route, establishing an efficient fecal oral transmission pathway that bypasses the mosquito vector. Infection induces typical clinical signs with 40% mortality. Viral replication occurs in the brain and spleen, with the cloaca serving as the primary shedding site for up to 28 days&amp;mdash;yielding significantly higher titers than pharyngeal swabs and indicating prolonged environmental contamination. Even a low dose (10&amp;sup3; TCID50) establishes infection, primarily restricted to the duodenum. Maternal antibodies prevent mortality but do not block viral replication. Critically, we uncover the mechanism that enables this cross species transition. Using single round infection particles and E swapped chimeric viruses (CQ/MM E and MM/CQ E), we show that specific interactions between a naturally isolated gut commensal bacterium (Enterococcus hirae&amp;nbsp;293) and the viral envelope (E) protein enhance viral thermostability. This bacterium mediated stabilization allows the virus to retain infectivity within the gastrointestinal tract and the external environment&amp;mdash;conditions fundamentally different from the mosquito vector environment. Thus, our results directly explain how an ancestral mosquito adapted&amp;nbsp;orthoflavivirus&amp;nbsp;can overcome the thermal and enzymatic barriers of the avian gut, enabling a switch from vector borne to fecal oral transmission in an avian host.</dc:description>
  <dc:subject>TMUV; Fecal–Oral Transmission; Vector Independence; Envelope (E) protein; Gut commensal bacteria; Viral thermostability</dc:subject>
  <dc:creator>Ailin Deng</dc:creator>
  <dc:creator>Shun Chen</dc:creator>
  <dc:creator>Zhen Wu</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
</oai_dc:dc>

    </metadata>
</record>
</GetRecord>
</OAI-PMH>