| Summary: | 碩士 === 國防醫學院 === 微生物及免疫學研究所 === 94 === Homologous interference is a phenomenon where a cell infected with a virus is resistant to superinfection by the same or similar virus, and such interference has been observed for a number of viruses. According to our previous research, Dengue virus could resist to a superinfection by homologous virus in a primary and persistent infection in mammalian and C6-36 (Aedes albopictus) cells. In this study, we investigated what causes homologous interference in flavivirus. During flavivirus productive replication, double-stranded RNA (dsNRA) intermediates and stem-loop secondary structures derived from certain regions of ssRNA genome are believed to be substantially generated in cytoplasm, which may induce cellular RNAi as a nucleic acid-based immunity leading to homologous interference. First, we found that Den2 replication could not suppress RNAi. Second, when use known RNAi suppressor to block induced RNAi, we observed that this strategy could not break homologous interference. Third, we found persistent infection did not affect the expression of individual flaviviral genes by transient transfection, and conversely, the transient expression flaviviral gene had no effects on the following flavivirus infection, indicating flavivirus single gene is not sufficient to cause homologous interference. JEV NS5 protein alone seems to promote Den2 virus spread and infection. Finally, we observed that protein tyrosine phosphatases (PTPs) inhibitor- sodium orthovanadate could not inhibit flavivirus interference, the result shown that homologous interference didn’t break by PTPs inhibitor. To sum up, our results suggest flavivirus interference may not involve the cellular RNAi response.
|
|---|
