Knockdown of hnRNP K significantly lowered viral yields and delayed viral RNA synthesis compared to negative-control siRNA, indicating hnRNP K participates in EV71 replication.
Does hnRNP K knockdown reduce viral replication in EV71-infected cells?
The cellular protein hnRNP K interacts with the EV71 5' UTR and is required for efficient viral replication, highlighting a potential target for antiviral therapy.
Enterovirus 71 (EV71) is a picornavirus that can cause severe neurological complications in children. Like other picornaviruses, the genomic RNA of EV71 contains a long 5' untranslated region (UTR). Cellular proteins interact with the EV71 5' UTR, and these interactions are important for virus replication. Using an RNA pull-down assay and proteomics approaches, this study identified the heterogeneous nuclear ribonucleoprotein K (hnRNP K) as one of the EV71 5' UTR-associated proteins. The interaction between hnRNP K and the 5' UTR was further confirmed by mapping the interaction regions to stem-loops I-II and IV in the 5' UTR. During EV71 infection, hnRNP K was enriched in the cytoplasm where virus replication occurs, whereas hnRNP K was localized in the nucleus in mock-infected cells. Viral yields were found to be significantly lower in hnRNP K knockdown cells and viral RNA synthesis was delayed in hnRNP K knockdown cells in comparison with negative-control cells treated with small interfering RNA. These results suggest that hnRNP K interacts with the EV71 5' UTR and participates in virus replication.
Lin et al. (2008) studied Enterovirus 71 infection. hnRNP K knockdown (siRNA) vs. Negative-control siRNA was evaluated on Viral yields and viral RNA synthesis. Knockdown of hnRNP K significantly lowered viral yields and delayed viral RNA synthesis compared to negative-control siRNA, indicating hnRNP K participates in EV71 replication.