Key result
Duck hepatitis A virus serotype 1 infection induced significant differences in apoptotic cells and apoptosis-related gene expression compared to controls.
Apoptosis appears to play an important role in duck hepatitis A virus serotype 1 infection, where its suppression may facilitate viral multiplication.
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May implicate apoptosis in duck viral hepatitis pathogenesis; leaves open whether modulating it affects outcomes in poultry.
To investigate the role of apoptosis in duck viral hepatitis pathogenesis, 4- and 21-d-old ducks were inoculated with duck hepatitis A virus serotype 1 and killed at 2, 6, 12, 24, and 48 h postinfection. TdT-mediated dUTP nick-end labeling was used to detect apoptosis cells. Expression profiles of apoptosis-related genes including caspase-3, -8, -9, and Bcl-2 in spleen, bursa of Fabricius, liver, and the quantity of virus in blood were examined using real-time PCR. The TdT-mediated dUTP nick-end labeling analysis indicated there was a significant difference of apoptotic cells between treatments and controls. The same difference also appeared in virus amount variation in blood during infection. Gene expression analysis revealed that the apoptosis-related gene expression profile was different in the 2 groups, and also different between various organs. This study suggested that apoptosis may play an important role in duck hepatitis A virus serotype 1 infection, and apoptosis suppression might facilitate virus multiplication, resulting in the highest virus concentration in the host.
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Sheng et al. (2014) studied Duck viral hepatitis. Duck hepatitis A virus serotype 1 inoculation vs. Controls was evaluated on Apoptotic cells and apoptosis-related gene expression. Duck hepatitis A virus serotype 1 infection induced significant differences in apoptotic cells and apoptosis-related gene expression compared to controls.
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