Experimental duck hepatitis B virus infection: pathology and evolution of hepatic and extrahepatic infection

• Published in: Hepatology (Baltimore, Md.) Vol. 8; no. 3; p. 507
• Main Authors: Freiman, J S, Jilbert, A R, Dixon, R J, Holmes, M, Gowans, E J, Burrell, C J, Wills, E J, Cossart, Y E
• Format: Journal Article
• Language: English
• Published: United States 01.05.1988
• Subjects: Animals; DNA, Viral - analysis; Ducks; Enterovirus Infections - metabolism; Enterovirus Infections - pathology; Enterovirus Infections - veterinary; Hepatitis B - etiology; Hepatitis B virus; Hepatitis, Viral, Animal - metabolism; Hepatitis, Viral, Animal - pathology; Humans; Immunohistochemistry; Kidney - metabolism; Kidney - pathology; Liver - metabolism; Liver - pathology; Microscopy, Electron; Nucleic Acid Hybridization; Pancreas - metabolism; Pancreas - pathology; Poultry Diseases - metabolism; Poultry Diseases - pathology; Spleen - metabolism; Spleen - pathology
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.1840080313

Seventy, 1-day-old ducklings inoculated intraperitoneally with duck hepatitis B virus and 30 controls have been studied over a 2-year period. Infection with duck hepatitis B virus occurred in all inoculated ducks, although this was not associated with clinical morbidity. Duck hepatitis B virus DNA was first detected in liver on Day 3, in pancreatic acinar cells on Day 4, serum on Day 6, splenic red and white pulp on Day 7 and in the renal glomurulus on Day 14, using a combination of dot, Southern blot and in situ hybridization techniques. Peak levels of circulating virus, as determined by DNA polymerase levels, occurred 1 to 4 weeks postinoculation. Mild degrees of portal inflammation were seen in sections of liver tissue in both infected and control ducks. However, moderately severe inflammatory changes were present in 8 of 22 infected birds compared with 0 of 18 controls (p less than 0.025). Appearance of this inflammatory infiltrate 6 weeks postinoculation coincided with a decrease in levels of duck hepatitis B virus DNA in hepatocytes and within the pancreatic acinar cells. At the same time, duck hepatitis B virus DNA became increasingly localized to the splenic germinal centers, and viral DNA was first detected in pancreatic islet cells. No histological changes accompanied the extra-hepatic tissue infection. The sequence and significance of duck hepatitis B virus infection in liver and extra-hepatic tissues is discussed in relation to the pathogenesis of hepatitis B virus infection in man.