| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 100 === Influenza virus is a well-known RNA virus which results in several global pandemic breakouts in history. Participation of host cellular factors is necessary for influenza virus replication and the mechanism of these host factors in virus replication is not fully understood. To investigate the mechanism of host factors involved in virus replication, we compared two references which performed large-screening for host factor using A549 cell and Flu A/WSN/33 virus strain and selected several potential host factors involved in virus replication, including FKBP8. Western blot analysis revealed that FKBP8 protein expression level was decreased during viral infection. Overexpression of FKBP8 followed by virus infection showed inhibition of viral protein and viral titers, and opposite results were observed when FKBP8 was silenced. Previous studied indicated that FKBP8 could regulate mTOR signaling pathway in which S6K, eEF2k and eIF4B was phosphorylated. The phosphorylation levels of S6K and eIF4B protein were increased after viral infection whereas expression of eEF2K was decreased. Furthermore, the phosphorylation level of S6K and eIF4B were upregulated and eEF2K was significantly downregulated after knockdown of FKBP8 prior to virus infection. The data indicated that influenza replication was regulated by FKBP8 expression through inhibition of some branches of mTOR signaling pathway.
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