Abstract:
:Enteric pathogens must overcome intestinal defenses to establish infection. In Drosophila, the ERK signaling pathway inhibits enteric virus infection. The intestinal microflora also impacts immunity but its role in enteric viral infection is unknown. Here we show that two signals are required to activate antiviral ERK signaling in the intestinal epithelium. One signal depends on recognition of peptidoglycan from the microbiota, particularly from the commensal Acetobacter pomorum, which primes the NF-kB-dependent induction of a secreted factor, Pvf2. However, the microbiota is not sufficient to induce this pathway; a second virus-initiated signaling event involving release of transcriptional paused genes mediated by the kinase Cdk9 is also required for Pvf2 production. Pvf2 stimulates antiviral immunity by binding to the receptor tyrosine kinase PVR, which is necessary and sufficient for intestinal ERK responses. These findings demonstrate that sensing of specific commensals primes inflammatory signaling required for epithelial responses that restrict enteric viral infections.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Sansone CL,Cohen J,Yasunaga A,Xu J,Osborn G,Subramanian H,Gold B,Buchon N,Cherry Sdoi
10.1016/j.chom.2015.10.010subject
Has Abstractpub_date
2015-11-11 00:00:00pages
571-81issue
5eissn
1931-3128issn
1934-6069pii
S1931-3128(15)00420-5journal_volume
18pub_type
杂志文章abstract::Eliciting HIV-1-specific broadly neutralizing antibodies (bNAbs) remains a challenge for vaccine development, and the potential of passively delivered bNAbs for prophylaxis and therapeutics is being explored. We used neutralization data from four large virus panels to comprehensively map viral signatures associated wi...
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journal_title:Cell host & microbe
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