| Summary: | 碩士 === 國立中興大學 === 生物醫學研究所 === 98 === Influenza A virus, the prototype of the Orthomyxoviridae family, spreads world-wide and results in seasonal epidemics. Among 11 viral proteins encoded by 8 negative template RNA segments, the non-structural protein NS1 of influenza A virus mediates viral mRNA translation and rRNA synthesis as well as regulates host innate immune response and other cellular signaling pathway through binding of RNA with its N-terminal or/and or proteins with it effecting domain. Cell death is a final result of virus infection and displays various features of cell facing stress and pathogensis invasion. Many virus proteins have been reported to regulate apoptosis, a programmed cell death either, for accelerating viral dispersion or for preventing premature viral production. To specify influenza virus-induced cell death, we observed that the deprivation of NS1 protein resulted in more severe in cell death during influenza A virus infection, in epithelial adherence, plasma membrane integrality, and nuclear macromolecule disorder manner. Meanwhile, we also found that the expression of NS1 might enhance polyIC-induced DNA laddering but slightly inhibited staurosporine induced DNA laddering. Moreover, the expression of NS1 protein was associated with vanishing PARP, the cleavage form of which is a hallmark of apoptosis. Through confocol laser scanning biological microscope, we detected that NS1 protein of influenza A virus localized at mitochondria. To sum, those data indicated that the NS1 of influenza virus might determine when and how host cells go to die. And together with the mitochondria localization of NS1 protein, we presume that NS1 mediates mitochondrial membrane permeability to regulate cell death.
|
|---|
