Journal article
Varicella-Zoster Virus Immediate-Early Protein ORF61 Abrogates the IRF3-Mediated Innate Immune Response through Degradation of Activated IRF3
Abstract
Varicella-zoster virus (VZV) infection of differentiated cells within the host and establishment of latency likely requires evasion of innate immunity and limits secretion of antiviral cytokines. Here we report that its immediate-early protein ORF61 antagonizes the beta interferon (IFN-β) pathway. VZV infection down-modulated the Sendai virus (SeV)-activated IFN-β pathway, including mRNA of IFN-β and its downstream interferon-stimulated genes …
Authors
Zhu H; Zheng C; Xing J; Wang S; Li S; Lin R; Mossman KL
Journal
Journal of Virology, Vol. 85, No. 21, pp. 11079–11089
Publisher
American Society for Microbiology
Publication Date
November 2011
DOI
10.1128/jvi.05098-11
ISSN
0022-538X
Associated Experts
Fields of Research (FoR)
Medical Subject Headings (MeSH)
Blotting, WesternCell LineHerpesvirus 3, HumanHumansImmune EvasionImmunity, InnateImmunoprecipitationInterferon Regulatory Factor-3Interferon-betaProteasome Endopeptidase ComplexProtein BindingProtein Interaction MappingReverse Transcriptase Polymerase Chain ReactionSendai virusUbiquitinViral Proteins