Cytokine gene expression in the livers of ducklings infected with duck hepatitis virus-1 JX strain

Abstract

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.

Cytokine storms are primarily responsible for the rapid death of ducklings infected with duck hepatitis A virus type 1

“…The CH strain caused nearly 50% mortality in ducklings and induced more efficient virus replication in the liver. Massive hemorrhages and necrotic lesions appeared on the liver surface with virus replication of the CH strain, which is consistent with previous reports in the literature 2,19,20 . Additionally, the presence of microscopic lesions revealed liver parenchyma infiltration by large numbers of red blood cells, and this effect was accompanied by hepatocyte necrosis and apoptosis corresponding to hemorrhages and necrotic lesions on the liver surface.…”

DNA Methylation and Regulation of the CD8A after Duck Hepatitis Virus Type 1 Infection

“…The death peak was approximately 36 h.p.i., and the mortality rate declined dramatically by 48 h.p.i. After 72 h.p.i., no duck deaths were observed, which is in agreement with data previously described in the literature [12]–[13].…”

“…It is mainly caused by duck hepatitis virus type 1 (DHV-1) [12]. It is the most widely distributed virus that can cause mortality rates above 90% in 1-week-old ducklings [13].…”

Effects of Bush Sophora Root polysaccharide and its sulfate on immuno-enhancing of the therapeutic DVH

“…The majority of hepadnaviruses induce the high level of serum IL-6 [24]. But no significant change is found in ducklings infected DHAV within a week [25]. A similar result was observed in the present study.…”