A homolog of the variola virus B22 membrane protein contributes to ectromelia virus pathogenicity in the mouse footpad model

Abstract Most poxviruses encode a homolog of a ~200,000-kDa membrane protein originally identified in variola virus. We investigated the importance of the ectromelia virus (ECTV) homolog C15 in a natural infection model. In cultured mouse cells, the replication of a mutant virus with stop codons nea...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2017-01, Vol.501, p.107-114
Main Authors: Reynolds, Sara E, Earl, Patricia L, Minai, Mahnaz, Moore, Ian, Moss, Bernard
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Ectromelia virus
Ectromelia virus - genetics
Ectromelia virus - metabolism
Ectromelia virus - pathogenicity
Ectromelia, Infectious - genetics
Ectromelia, Infectious - metabolism
Ectromelia, Infectious - pathology
Ectromelia, Infectious - virology
Female
Host defense
Humans
Infectious Disease
Innate immunity
Liver - pathology
Liver - virology
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mice, Inbred BALB C
Poxvirus
Spleen - pathology
Spleen - virology
T cells
Variola virus - genetics
Variola virus - metabolism
Viral pathogenicity
Viral Proteins - genetics
Viral Proteins - metabolism
Virulence
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Summary:Abstract Most poxviruses encode a homolog of a ~200,000-kDa membrane protein originally identified in variola virus. We investigated the importance of the ectromelia virus (ECTV) homolog C15 in a natural infection model. In cultured mouse cells, the replication of a mutant virus with stop codons near the N-terminus (ECTV-C15Stop) was indistinguishable from a control virus (ECTV-C15Rev). However, for a range of doses injected into the footpads of BALB/c mice there was less mortality with the mutant. Similar virus loads were present at the site of infection with mutant or control virus whereas there was less ECTV-C15Stop in popliteal and inguinal lymph nodes, spleen and liver indicating decreased virus spread and replication. The latter results were supported by immunohistochemical analyses. Decreased spread was evidently due to immune modulatory activity of C15, rather than to an intrinsic viral function, as the survival of infected mice depended on CD4+ and CD8+ T cells.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2016.11.010