Key result
DHV-1 JX infection in ducklings triggers biphasic inflammation with ~128-fold higher IFN-α and elevated ALT.
Why the study?
Duck hepatitis virus type 1 causes severe liver disease and high mortality in ducklings, but the hepatic cytokine gene expression response to infection is not well characterized.
Biphasic cytokine expression marks acute DHV-1 liver injury in ducklings; leaves open immunomodulatory targets for future intervention studies.
Duck hepatitis virus type 1 (DHV-1) causes a highly contagious disease in ducklings and is often associated with liver necrosis, hemorrhages, and high mortality. In the current study, the expression levels of gene transcripts encoding proinflammatory cytokines and the virus were measured by quantitative reverse-transcription PCR in duck livers after infection with a DHV-1 JX isolate obtained from natural cases in Hubei Province, China. In addition, sera IL-1β, IL-6, and alanine aminotransferase levels were quantified. Liver histopathology was examined following DHV-1 infection. The ducklings died within 1 to 2 d postinfection (d.p.i.) because of typical liver degeneration, hemorrhage, necrosis, and bile-duct epithelial cell proliferation. Transcripts of the cytokines IFN-α, IL-6, TNF-α, and IL-10 decreased by 0.5 d.p.i. and then gradually increased at 1 d.p.i. Similarly, DHV-1 JX 3D gene levels in the liver sharply increased at 1 d.p.i. and then maintained a high level. In contrast, liver TNF-α and IL-1β transcripts showed no increased expression of the cytokine gene postinfection and significantly decreased compared with the expression at 0.25 d.p.i., only the expression of IFN-α transcripts increased 128-fold by 1 d.p.i. Changes in the serum IL-6 level remained relatively stable postinfection and not significantly different compared with that of the control (P > 0.05), whereas serum levels of IL-1β significantly decreased at 0.5 d.p.i. and increased from 1 d.p.i. onwards (P < 0.05). Serum alanine aminotransferase levels significantly increased 2 d.p.i. compared with that of the control group (P < 0.01), which seemed to keep with the number of dead ducks. The cytokines exhibited a biphasic pattern following DHV-1 JX infection. Taken together, the data indicated that duckling liver inflammatory responses were produced following experimental DHV-1 JX infection involving multiple cytokines.
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Gu et al. (2012) studied Duck hepatitis virus type 1 (DHV-1) infection. Duck hepatitis virus-1 JX strain infection vs. Uninfected control group was evaluated on Liver cytokine gene expression and serum alanine aminotransferase levels. Experimental DHV-1 JX infection in ducklings induced a biphasic inflammatory response, including a 128-fold increase in IFN-α transcripts by 1 day postinfection and significantly elevated ALT (P<0.01).
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