Journal article Open Access

A STING-dependent innate-sensing pathway mediates resistance to corneal HSV-1 infection via upregulation of the antiviral effector tetherin

Royer, D. J.; Carr, D. J. J.


DataCite XML Export

<?xml version='1.0' encoding='utf-8'?>
<resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd">
  <identifier identifierType="URL">https://zenodo.org/record/883748</identifier>
  <creators>
    <creator>
      <creatorName>Royer, D. J.</creatorName>
      <givenName>D. J.</givenName>
      <familyName>Royer</familyName>
    </creator>
    <creator>
      <creatorName>Carr, D. J. J.</creatorName>
      <givenName>D. J. J.</givenName>
      <familyName>Carr</familyName>
    </creator>
  </creators>
  <titles>
    <title>A STING-dependent innate-sensing pathway mediates resistance to corneal HSV-1 infection via upregulation of the antiviral effector tetherin</title>
  </titles>
  <publisher>Zenodo</publisher>
  <publicationYear>2015</publicationYear>
  <dates>
    <date dateType="Issued">2015-12-02</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://zenodo.org/record/883748</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1038/mi.2015.124</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">Type 1 interferons (IFNα/β) mediate immunologic host resistance to
numerous viral infections including herpes simplex virus type 1 (HSV-1). The
pathways responsible for maintenance of IFNα/β signaling during the innate
immune response to acute HSV-1 infection in the cornea are incompletely
understood. Using a murine ocular infection model, we hypothesized that the
stimulator of IFN genes (STING) mediates host resistance to HSV-1 infection in
the external ocular surface and preserves the structural integrity of this immune
privileged mucosal site. Viral pathogenesis, tissue pathology, and host immune
responses during ocular HSV-1 infection were evaluated and characterized by
plaque assay, esthesiometry, pachymetry, immunohistochemistry, flow
cytometry, and siRNA transfection in wildtype C57BL/6 (WT), STING-deficient
(STING-/-), and IFNα/β receptor-deficient (CD118-/-) mice at days 3-5 post
infection (pi). The presence of STING was critical for sustained control of HSV-1
replication in the corneal epithelium and neuroinvasion, but loss of STING had a
negligible impact with respect to gross tissue pathology. Auxiliary STING
independent IFNα/β signaling pathways were responsible for maintenance of the
corneal integrity. Lymphatic vessels, mast cells, and sensory innervation were
compromised in CD118-/- mice concurrent with increased tissue edema. STING
dependent signaling led to the upregulation of tetherin, a viral restriction factor
we identify to be important in containing the spread of HSV-1 in vivo.</description>
  </descriptions>
</resource>
137
51
views
downloads
Views 137
Downloads 51
Data volume 662.5 MB
Unique views 131
Unique downloads 51

Share

Cite as