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The Early Host Innate Immune Response to Duck Hepatitis B Virus Infection

¹ The University of Sydney;
² The University of New South Wales

³ E-mail: kvickery{at}infdis.usyd.edu.au

The early phase after hepatitis B virus infection could play a crucial role in clearance and/or persistence of the virus, particularly in neonates. This work compared the early phase of duck hepatitis B virus infection in day old (D1) and 28 day old (D28) ducks to determine whether differences in viral or host innate immune response can be related to the difference in outcome. In the first phase almost immediately after inoculation virus was taken up by components of the reticulo-endothelial systems, particularly liver-specific macrophages, Kupffer cells. Very early after infection the induction of interferon alpha by infected hepatocytes occurs and was rapidly reinforced by recruitment of effector lymphocytes which directly or indirectly cause apoptosis eliminating infected hepatocytes as was seen in mature birds. In addition, a lack of lymphocytic infiltration of the liver was found in D1 ducks which supports the suggestion that the innate immune network is less effective in D1 ducks. Taken together these results suggest that failure of the co-ordinated innate immune response rather than a defect in induced anti-viral cell mediated immunity may be the key factor which makes baby ducks vulnerable to persistence of hepadnavirus infection.

Received 30 July 2009; accepted 19 October 2009.