Abstract
Rotavirus is a primary cause of severe dehydrating gastroenteritis in infants and young children. The virus is sensitive to the antiviral effects triggered by the interferon (IFN)-signaling pathway, an important component of the host cell innate immune response. To counteract these effects, rotavirus encodes a nonstructural protein (NSP1) that induces the degradation of proteins involved in regulating IFN expression, such as members of the IFN regulatory factor (IRF) family. In some instances, NSP1 also subverts IFN expression by causing the degradation of a component of the E3 ubiquitin ligase complex responsible for activating NF-κB. By antagonizing multiple components of the IFN-induction pathway, NSP1 aids viral spread and contributes to rotavirus pathogenesis.
Highlights
The innate immune system provides an immediate mechanism of suppressing the replication and spread of viruses
The interaction of viral nucleic acids with pattern-recognition receptors (PRRs) leads to the activation of IFN regulatory factors (IRFs) and nuclear factor (NF)- B, which translocate from the cytoplasm to the nucleus where they stimulate transcription of type I IFN genes
The analysis revealed that NSP1 of diverse origins bound to IRF3
Summary
The innate immune system provides an immediate mechanism of suppressing the replication and spread of viruses. The interaction of viral nucleic acids with PRRs leads to the activation of IFN regulatory factors (IRFs) and nuclear factor (NF)- B, which translocate from the cytoplasm to the nucleus where they stimulate transcription of type I IFN genes. IRF7 is present in most cells at very low levels, and its expression is amplified by type I IFN [7,8] Both IRF3 and IRF7 reside in an inactive state in the cytoplasm and are activated by phosphorylation of residues in the C-terminal regulatory region by the kinases TBK1 or IKK- [9,10]. Secreted type I IFNs bind to type I IFN receptors (IFNAR) and induce the formation of IFN-stimulated gene factor 3 (ISGF3), a heterotrimeric complex consisting of signal transducer and activator of transcription (STAT) 1, STAT2, and IRF9. Some RV NSP1 proteins inhibit the type I IFN response by degrading IRF3 and IRF7, while at least one NSP1 prevents type I IFN induction by degrading -TrCP and preventing the nuclear translocation of NF- B
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