Topic
NS5B
About: NS5B is a research topic. Over the lifetime, 1314 publications have been published within this topic receiving 59534 citations.
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TL;DR: In this article, the authors have identified a principal bioactive component ''corilagin'' which showed significant inhibition of the HCV key enzymes, NS3 protease and NS5B RNA-dependent-RNA-polymerase.
36 citations
TL;DR: It is found that human eukaryotic initiation factor 4AII (heIF4AII), which is a component of the eIF4F complex and RNA-dependent ATPase/helicase, interacted with NS5B protein, which raises the possibility that heIF4 aII facilitates the genomic RNA synthesis of NS5 B protein by unwinding the secondary structure of the HCV genome.
36 citations
TL;DR: Analysis of residue interaction network (RIN) of the complexes between the drugs with wild-type and the mutant polymerase found that the mutation residues in the networks involved in the drug resistance possessed a relatively lower size of topology centralities.
36 citations
TL;DR: It is indicated that the 3' CCCGG sequence of the plus-strand 3' UTR, and the3' CATATGCTC fragment of the minus-stranded RNA are essential to in vitro synthesis of theminus-Strand RNA and the plus'-strand RNA, respectively.
Abstract: The NS5B protein of the classical swine fever virus (CSFV) is the RNA-dependent RNA polymerase of the virus and is able to catalyze the viral genome replication. The 3' untranslated region is most likely involved in regulation of the Pestivirus genome replication. However, little is known about the interaction between the CSFV NS5B protein and the viral genome. We used different RNA templates derived from the plus-strand viral genome, or the minus-strand viral genome and the CSFV NS5B protein obtained from the Escherichia coli expression system to address this problem. We first showed that the viral NS5B protein formed a complex with the plus-strand genome through the genomic 3' UTR and that the NS5B protein was also able to bind the minus-strand 3' UTR. Moreover, it was found that viral NS5B protein bound the minus-strand 3' UTR more efficiently than the plus-strand 3' UTR. Further, we observed that the plus-strand 3' UTR with deletion of CCCGG or 21 continuous nucleotides at its 3' terminal had no binding activity and also lost the activity for initiation of minus-strand RNA synthesis, which similarly occurred in the minus-strand 3' UTR with CATATGCTC or the 21 nucleotide fragment deleted from the 3' terminal. Therefore, it is indicated that the 3' CCCGG sequence of the plus-strand 3' UTR, and the 3' CATATGCTC fragment of the minus-strand are essential to in vitro synthesis of the minus-strand RNA and the plus-strand RNA, respectively. The same conclusion is also appropriate for the 3' 21 nucleotide terminal site of both the 3' UTRs.
36 citations
TL;DR: It is suggested that the three species of siRNAs can efficiently inhibit CSFV genome replication and infectious virus production, with the inhibition persisting for 72-84 h.
36 citations