Study on the Mechanism That Mosquito Cells Sruvive Dengue 2 Virus Infection

Dengue virus, a member of the family Flaviviridae, has been one of important mosquito-borne diseases in many tropical and subtropical countries, causing dengue fever and occasionally dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). The genome of dengue virus contains a single-stranded positive-sense RNA, with ~11 kilobases (kb) in length. The viral RNA, within host cells, directly translates into a single polyprotein that is subsequently cleaved into three structural proteins and seven nonstructural proteins. Hypothetically, viruses invading a host cell redirect cellular processes to meet the needs of viral propagation, leading to the induction of novel changes in gene expression. Previous observations revealed that dengue viruses cause trivial deleterious effects to infected mosquito cells and frequently lead to persistent infection. On the other hand, the infection frequently induces apoptosis in vertebrate cells, suggesting that host-virus interactions are relatively distinct in different combinations of viruses and host cells. Virus-induced apoptosis mediated by the unfolded protein response (UPR) has been hypothesized as a crucial pathogenic event in viral infection of mammalian cells; which creates conditions beneficial to the viral replication eventually. It is still ambiguous that how mosquito cells act, especially at the gene level, during infection by dengue viruses. As a result, it is interesting and worthwhile to have a whole profile of gene expression in response to virus infection in mosquito cells. In order to accomplish this goal, in this study, gene expression changed during virus infection in C6/36 cells will be extensively investigated; from which genes highly related to cell survival will be identified and investigated for their roles during the infection by dengue 2 virus.

Project ID:PD10101-0452
External Project ID:NSC100-2313-B182-001-MY3