病毒mRNA合成
中文名称
通路描述
与宿主细胞mRNA类似，流感病毒mRNA均具有5'帽和3'多聚腺苷酸化（参见Neumann, 2004）。然而，甲基化的帽被从宿主细胞mRNA中清除，作为病毒RNA合成的引物，这一过程称为“帽跳跃”（参见Krug, 1981; Hagen, 1994）。PB2聚合酶蛋白结合帽，激活PB1对宿主mRNA的内切酶切割。病毒mRNA的3'多聚腺苷酸化通量由聚合酶在模板vRNA 5'端附近的poly-U通量上的停滞产生（参见Robertson, 1981; Zheng, 1999）。第二个过程允许在宿主细胞多聚腺苷酸化过程被抑制时进行病毒mRNA的多聚腺苷酸化（参见Engelhardt, 2006; Amorim, 2006）。值得注意的是，早期转录本（包括NP和NS1）在晚期转录本（M1、HA和NS2）积累于细胞质之前，且在不同丰度下，表明存在额外的机制调节病毒基因表达（参见Shapiro, 1987; Hatada, 1989; Amorim, 2006）。
英文描述
Viral Messenger RNA Synthesis Like the mRNAs of the host cell, influenza virus mRNAs are capped and polyadenylated (reviewed in Neumann, 2004). The methylated caps, however, are scavenged from host cell mRNAs and serve as primers for viral RNA synthesis, a process termed 'cap-snatching' (Krug, 1981; Hagen, 1994). The PB2 polymerase protein binds the cap, activating endonucleolytic cleavage of the host mRNA by PB1. The 3' poly-A tracts on viral messages are generated by polymerase stuttering on poly-U tracts near the 5' end of the template vRNA (Robertson, 1981; Zheng, 1999). The second process allows polyadenylation of viral mRNAs when the host cell polyadenylation process has been inhibited (Engelhardt, 2006; Amorim, 2006). Notably, early transcripts (including NP and NS1) accumulate in the cytoplasm before late transcripts (M1, HA, and NS2), and in varying abundances, suggesting additional control mechanisms regulating viral gene expression (Shapiro, 1987; Hatada, 1989; Amorim, 2006).
所含基因
45 个基因