Zheng H, Lee H A, Palese P, García-Sastre A
Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
J Virol. 1999 Jun;73(6):5240-3. doi: 10.1128/JVI.73.6.5240-5243.1999.
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.
流感病毒是一种负链RNA病毒,其病毒聚合酶被认为是通过在靠近病毒RNA模板5'端的一段五到七个尿苷残基处发生错读来对mRNA进行聚腺苷酸化的。然而,基于聚(A)尾的模板非依赖性合成的聚腺苷酸化机制尚未被排除。在本报告中,我们提供了新的证据,表明病毒聚合酶在RNA复制过程中在病毒RNA模板的聚(U)区段处发生错读的内在能力。已鉴定出在聚(U)区段处具有1至13个核苷酸长插入的变体。这些结果支持流感病毒mRNA聚腺苷酸化的错读机制。