Journal
MICROBIOLOGY AND IMMUNOLOGY
Volume 65, Issue 11, Pages 481-491Publisher
WILEY
DOI: 10.1111/1348-0421.12933
Keywords
apoptosis; duck Tembusu virus; Japanese encephalitis virus; primary duck neuron
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The study compared the infection mechanisms and cell death processes of DTMUV and JEV on duck neurons and fibroblasts, finding that DTMUV infection caused more intense apoptosis and suggesting that its induced immune response may be more toxic.
Duck Tembusu virus (DTMUV) and Japanese encephalitis virus (JEV) are mosquito-borne flaviviruses. These two viruses infect ducks; however, they show different neurological outcomes. The mechanism of DTMUV- and JEV-induced neuronal death has not been well investigated. In the present study examined the differences in the mechanisms involved in virus-induced cell death and innate immune responses between the DTMUV KPS54A61 strain and the JEV JaGAr-01 strain using primary duck neurons (DN) and duck fibroblasts (CCL-141). DN and CCL-141 were permissive for the infection and replication of these two viruses, which up-regulated the expression of innate immunity genes. Both DTMUV and JEV induced cell death via a caspase-3-dependent manner; however, DTMUV triggered more cell death than did JEV in both CCL-141 and DN. These findings suggest that DTMUV infection causes apoptosis in duck neurons and fibroblasts more strongly than JEV. The levels of the mRNA expression of innate immunity-related genes after DTMUV infection were generally higher than the levels after JEV infection, suggesting that DTMUV-induced immune response in duck cells may exhibit toxic effects rather than protective effects.
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