Key result
Influenza A virus RNA polymerase has the inherent ability to stutter at the poly(U) stretch of a viral RNA template during RNA replication, supporting a stuttering mechanism for polyadenylation.
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May guide antiviral development targeting viral polymerase; leaves open in vivo validation and clinical translation.
The viral polymerase of influenza virus, a negative-strand RNA virus, is believed to polyadenylate the mRNAs by stuttering at a stretch of five to seven uridine residues which are located close to the 5' ends of the viral RNA templates. However, a mechanism of polyadenylation based on a template-independent synthesis of the poly(A) tail has not been excluded. In this report, we present new evidence showing the inherent ability of the viral polymerase to stutter at the poly(U) stretch of a viral RNA template during RNA replication. Variants which possess 1- to 13-nucleotide-long insertions at the poly(U) stretch have been identified. These results support a stuttering mechanism for the polyadenylation of influenza virus mRNAs.
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Zheng et al. (1999) studied Influenza A virus. Influenza A virus RNA polymerase was evaluated on Mechanism of polyadenylation. Influenza A virus RNA polymerase has the inherent ability to stutter at the poly(U) stretch of a viral RNA template during RNA replication, supporting a stuttering mechanism for polyadenylation.
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