Key result
Seneca Valley virus 3Cpro cleaves heterogeneous nuclear ribonucleoprotein K at residue Q364, and the expression of the cleavage fragment facilitates viral replication.
Why the study?
Seneca Valley virus has emerged as an important pathogen threatening the global swine industry, and hnRNP K plays an important role in viral infection.
Population
Cultured cells
Design
In vitro laboratory study
Authors
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SVV 3Cpro may be an antiviral target; hypothesis-generating in animal models, clinical translation untested.
SVV 3C protease cleaves host hnRNP K to promote viral replication, identifying a potential antiviral target for SVV infection.
Song et al. (2022) studied Seneca Valley Virus infection. Seneca Valley Virus (SVV) infection and 3Cpro expression vs. Mock infection or empty vector was evaluated on Cleavage, degradation, and cytoplasmic redistribution of hnRNP K and viral replication. Seneca Valley virus 3Cpro cleaves heterogeneous nuclear ribonucleoprotein K at residue Q364, and the expression of the cleavage fragment facilitates viral replication.
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