急性呼吸道感染导致全世界的发病率和死亡率。这种致命疾病的常见原因是病毒,最常见的是流感病毒。流感病毒有几种感染能力,包括利用宿主的机器在细胞内生存和安全复制。这篇综述旨在研究有关流感病毒如何使用宿主机制的文献,包括内吞和自噬,它们在细胞内的内化和复制。这种审查方法涉及通过检查PubMed和Scopus数据库中发表的文章进行文献检索。使用的关键词是\"内吞\"或\"自噬\"和\"流感病毒\"。由于纳入和排除标准,纳入了18篇文章。GTPases开关,V-ATPase在流感病毒侵入宿主细胞的内吞机制中起关键作用。另一方面,LC3和Atg5通过自噬途径促进流感诱导的细胞凋亡。总之,流感病毒主要使用网格蛋白介导的内吞作用进入细胞,并通过退出内体转移到细胞核进行复制来避免在内体成熟过程中的降解。它还利用自噬诱导细胞凋亡以继续复制。流感病毒劫持内吞作用和自噬机制的能力可能是进一步研究的关键点。因此,我们讨论了流感病毒如何同时利用内吞和自噬,以及针对这些机制的新策略疗法的方法。
Acute respiratory infections contribute to morbidity and mortality worldwide. The common cause of this deadly disease is a virus, and one of the most commonly found is the influenza virus. Influenza viruses have several capabilities in infection, including utilizing the host\'s machinery to survive within cells and replicate safely. This review aims to examine the literature on how influenza viruses use host machinery, including
endocytosis and autophagy, for their internalization and replication within cells. This review method involves a literature search by examining articles published in the PubMed and Scopus databases. The keywords used were \"
Endocytosis\" OR \"Autophagy\" AND \"Influenza Virus\". Eighteen articles were included due to inclusion and exclusion criteria. GTPases switch, and V-ATPase plays a key role in the endocytic machinery hijacked by influenza viruses to enter host cells. On the other hand, LC3 and Atg5 facilitate influenza-induced apoptosis via the autophagic pathway. In conclusion, influenza viruses primarily use clathrin-mediated
endocytosis to enter cells and avoid degradation during endosomal maturation by exiting endosomes for transfer to the nucleus for replication. It also uses autophagy to induce apoptosis to continue replication. The capability of the influenza viruses to hijack
endocytosis and autophagy mechanisms could be critical points for further research. Therefore, we discuss how the influenza virus utilizes both
endocytosis and autophagy and the approach for a new strategic therapy targeting those mechanisms.