Herpes simplex virus 1 infection dampens the immediate early antiviral innate immunity signaling from peroxisomes by tegument protein VP16

dc.contributor.authorZheng, Chunfu
dc.contributor.authorSu, Chenhe
dc.date.accessioned2018-09-26T12:10:30Z
dc.date.available2018-09-26T12:10:30Z
dc.date.issued2017-02-21
dc.date.updated2018-09-26T12:10:30Z
dc.description.abstractAbstract Background Herpes simplex virus 1 (HSV-1) is an archetypal member of the alphaherpesvirus subfamily with a large genome encoding over 80 proteins, many of which play a critical role in virus-host interactions and immune modulation. Upon viral infections, the host cells activate innate immune responses to restrict their replications. Peroxisomes, which have long been defined to regulate metabolic activities, are reported to be important signaling platforms for antiviral innate immunity. It has been verified that signaling from peroxisomal MAVS (MAVS-Pex) triggers a rapid interferon (IFN) independent IFN-stimulated genes (ISGs) production against invading pathogens. However, little is known about the interaction between DNA viruses such as HSV-1 and the MAVS-Pex mediated signaling. Results HSV-1 could activate the MAVS-Pex signaling pathway at a low multiplicity of infection (MOI), while infection at a high MOI dampens MAVS-Pex induced immediately early ISGs production. A high-throughput screen assay reveals that HSV-1 tegument protein VP16 inhibits the immediate early ISGs expression downstream of MAVS-Pex signaling. Moreover, the expression of ISGs was recovered when VP16 was knockdown with its specific short hairpin RNA. Conclusion HSV-1 blocks MAVS-Pex mediated early ISGs production through VP16 to dampen the immediate early antiviral innate immunity signaling from peroxisomes.
dc.identifier.citationVirology Journal. 2017 Feb 21;14(1):35
dc.identifier.doihttps://doi.org/10.1186/s12985-017-0709-5
dc.identifier.urihttp://hdl.handle.net/1880/108019
dc.language.rfc3066en
dc.rights.holderThe Author(s).
dc.titleHerpes simplex virus 1 infection dampens the immediate early antiviral innate immunity signaling from peroxisomes by tegument protein VP16
dc.typeJournal Article
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