Wanitchang Asawin, Narkpuk Jaraspim, Jaru-ampornpan Peera, Jengarn Juggagarn, Jongkaewwattana Anan
Virology and Cell Technology Laboratory, National Center for Genetic Engineering and Biotechnology, Pathumthani 12120, Thailand.
Virology. 2012 Oct 10;432(1):194-203. doi: 10.1016/j.virol.2012.06.016. Epub 2012 Jul 6.
Given that co-infection of cells with equivalent titers of influenza A and B viruses (FluA and FluB) has been shown to result in suppression of FluA growth, it is possible that FluB-specific proteins might hinder FluA polymerase activity and replication. We addressed this possibility by individually determining the effect of each gene of FluB on the FluA polymerase assay and found that the nucleoprotein of FluB (NP(FluB)) inhibits polymerase activity of FluA in a dose-dependent manner. Mutational analyses of NP(FluB) suggest that functional NP(FluB) is necessary for this inhibition. Slower growth of FluA was also observed in MDCK cells stably expressing NP(FluB). Further analysis of NP(FluB) indicated that it does not affect nuclear import of NP(FluA). Taken together, these findings suggest a novel role of NP(FluB) in inhibiting replication of FluA, providing more insights into the mechanism of interference between FluA and FluB and the lack of reassortants between them.
鉴于已证明用等量滴度的甲型和乙型流感病毒（FluA和FluB）共同感染细胞会导致FluA生长受到抑制，因此FluB特异性蛋白可能会阻碍FluA聚合酶活性和复制。我们通过分别确定FluB每个基因对FluA聚合酶测定的影响来探讨这种可能性，发现FluB的核蛋白（NP(FluB)）以剂量依赖的方式抑制FluA的聚合酶活性。对NP(FluB)的突变分析表明，功能性NP(FluB)是这种抑制所必需的。在稳定表达NP(FluB)的MDCK细胞中也观察到FluA生长较慢。对NP(FluB)的进一步分析表明，它不影响NP(FluA)的核输入。综上所述，这些发现表明NP(FluB)在抑制FluA复制中具有新作用，为FluA和FluB之间的干扰机制以及它们之间缺乏重配体提供了更多见解。
