Virology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Road, New Delhi, India.
Med Sci Monit. 2011 Jun;17(6):RA148-54. doi: 10.12659/msm.881801.
Influenza viruses comprise a major class of human respiratory pathogens, responsible for causing morbidity and mortality worldwide. Influenza A virus, due to its segmented RNA genome, is highly subject to mutation, resulting in rapid formation of variants. During influenza infection, viral proteins interact with host proteins and exploit a variety of cellular pathways for their own benefit. Influenza virus inhibits the synthesis of these cellular proteins and facilitates expression of its own proteins for viral transcription and replication. Infected cell pathways are hijacked by an array of intracellular signaling cascades such as NF-κB signaling, PI3K/Akt pathway, MAPK pathway, PKC/PKR signaling and TLR/RIG-I signaling cascades. This review presents a research update on the subject and discusses the impact of influenza viral infection on these cell signaling pathways.
流感病毒是一类主要的人类呼吸道病原体,在全球范围内可导致发病和死亡。由于其 RNA 基因组分段,甲型流感病毒极易发生突变,导致变体迅速形成。在流感感染过程中,病毒蛋白与宿主蛋白相互作用,并利用多种细胞途径为自身谋取利益。流感病毒抑制这些细胞蛋白的合成,并促进其自身蛋白的表达,以进行病毒转录和复制。受感染细胞途径被一系列细胞内信号级联反应所劫持,如 NF-κB 信号、PI3K/Akt 通路、MAPK 通路、PKC/PKR 信号和 TLR/RIG-I 信号通路。本综述介绍了该领域的最新研究进展,并讨论了流感病毒感染对这些细胞信号通路的影响。