Vaccinia Virus CrmE Encodes a Soluble and Cell Surface Tumor Necrosis Factor Receptor That Contributes to Virus Virulence

Poxviruses encode soluble cytokine receptors to interfere with host immune functions. Cells infected with vaccinia virus (VV) strains USSR, Lister, and Evans express soluble and cell surface tumor necrosis factor receptors (vTNFRs). We have characterized vTNFR activity in VV USSR and identified an o...

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Published inVirology (New York, N.Y.) Vol. 292; no. 2; pp. 285 - 298
Main Authors Reading, Patrick C., Khanna, Anu, Smith, Geoffrey L.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 20.01.2002
Subjects
Animals
Apoptosis
Cell Line
cell surface
cowpox virus
CrmE protein
Female
Gene Deletion
Humans
lymphotoxin α
Mice
Mice, Inbred BALB C
Molecular Sequence Data
necrosis
Rats
Receptors, Tumor Necrosis Factor - genetics
Receptors, Tumor Necrosis Factor - metabolism
tumor necrosis factor
Vaccinia - physiopathology
Vaccinia - virology
Vaccinia virus
Vaccinia virus - genetics
Vaccinia virus - metabolism
Vaccinia virus - pathogenicity
Viral Proteins - genetics
Viral Proteins - metabolism
Virulence
virulence factors
cowpox virus
tumor necrosis factor
virulence
lymphotoxin α
necrosis
cell surface
apoptosis
vaccinia virus
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Summary:Poxviruses encode soluble cytokine receptors to interfere with host immune functions. Cells infected with vaccinia virus (VV) strains USSR, Lister, and Evans express soluble and cell surface tumor necrosis factor receptors (vTNFRs). We have characterized vTNFR activity in VV USSR and identified an open reading frame that encodes both soluble and cell surface activity, hereafter referred to as VV cytokine response modifier E (VV CrmE). Expression and characterization from recombinant VV and baculovirus showed VV CrmE to be an 18-kDa protein that bound human, mouse, and rat TNF-α, but not human LTα. VV CrmE inhibited the cytotoxic and apoptotic activities of human, but not mouse or rat, TNF in vitro. Nonetheless, in a murine intranasal model, USSR recombinants lacking CrmE were attenuated, demonstrating a role in vivo. Furthermore, expression of VV or cowpox virus vTNFRs from VV strain WR (which itself does not express a vTNFR) was shown to enhance virulence in the murine model.
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ISSN:0042-6822
1096-0341
DOI:10.1006/viro.2001.1236