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PKACs attenuate innate antiviral response by phosphorylating VISA and priming it for MARCH5-mediated degradation.

Abstract：

:Sensing of viral RNA by RIG-I-like receptors initiates innate antiviral response, which is mediated by the central adaptor VISA. How the RIG-I-VISA-mediated antiviral response is terminated at the late phase of infection is enigmatic. Here we identified the protein kinase A catalytic (PKAC) subunits α and β as negative regulators of RNA virus-triggered signaling in a redundant manner. Viral infection up-regulated cellular cAMP levels and activated PKACs, which then phosphorylated VISA at T54. This phosphorylation abrogated virus-induced aggregation of VISA and primed it for K48-linked polyubiquitination and degradation by the E3 ligase MARCH5, leading to attenuation of virus-triggered induction of downstream antiviral genes. PKACs-deficiency or inactivation by the inhibitor H89 potentiated innate immunity to RNA viruses in cells and mice. Our findings reveal a critical mechanism of attenuating innate immune response to avoid host damage at the late phase of viral infection by the house-keeping PKA kinase.

journal_name

PLoS Pathog

journal_title

PLoS pathogens

authors

Yan BR,Zhou L,Hu MM,Li M,Lin H,Yang Y,Wang YY,Shu HB

doi

10.1371/journal.ppat.1006648

subject

Has Abstract

pub_date

2017-09-21 00:00:00

pages

e1006648

issue

9

eissn

1553-7366

issn

1553-7374

pii

PPATHOGENS-D-17-01352

journal_volume

13

pub_type

杂志文章

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