Key result
hnRNP K acts as a host restriction factor that hinders PEDV replication by degrading the nucleocapsid protein and activates the interferon signaling pathway via MyD88 upregulation.
Why the study?
PEDV continues to cause epidemic and endemic outbreaks, necessitating investigation into host antiviral factors and immune mechanisms to elucidate effective antiviral strategies.
Does hnRNP K inhibit Porcine Epidemic Diarrhea Virus (PEDV) replication?
Does hnRNP K inhibit Porcine Epidemic Diarrhea Virus (PEDV) replication?
hnRNP K acts as a novel host restriction factor against PEDV by degrading viral nucleocapsid protein and activating the interferon signaling pathway.
The spread of the highly virulent PEDV in many countries is still leading to several epidemic and endemic outbreaks. To elucidate effective antiviral mechanisms, it is important to study the relationship between host antiviral factors and the virus and to investigate the mechanisms underlying host immune response against PEDV infection. In the work, we detected hnRNP K as a new host restriction factor which can hinder PEDV replication through degrading the nucleocapsid protein based on E3 ubiquitin ligase MARCH8 and the cargo receptor NDP52. In addition, via the upregulation of MyD88 expression, hnRNP K could also activate the interferon (IFN) signaling pathway. This study describes a previously unknown antiviral function of hnRNP K and offers a new vision toward host antiviral factors that regulate innate immune response as well as a protein degradation pathway against PEDV infection.
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Qin et al. (2022) studied Porcine Epidemic Diarrhea Virus (PEDV) infection. hnRNP K was evaluated on PEDV replication and type I IFN production. hnRNP K acts as a host restriction factor that hinders PEDV replication by degrading the nucleocapsid protein and activates the interferon signaling pathway via MyD88 upregulation.
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