Overexpression of hepatitis delta antigen protects insect cells from baculovirus-induced cytolysis.

Abstract

Hepatitis delta virus (HDV) is a human pathogen causing fulminant hepatitis and liver cirrhosis. HDV has a circular single-stranded RNA genome, which encodes only a single protein, hepatitis delta antigen (HDAg), from the antigenomic strand. Although the functional roles of HDAg have been extensively studied, the molecular mechanism of persistent infection and pathogenesis of HDV are not yet understood. Here we report that overexpressed HDAg protects cells from death in baculovirus-infected insect cells. Using both wild-type and recombinant baculovirus-infected insect cells, we have demonstrated that HDAg inhibited wild-type baculovirus-induced cytolysis and thus extended the survival of virus-infected insect cells. By deletion analysis, we show that N-terminal 25 amino acids are essential for this function. From these data, we suggest that HDAg may play a major role in persistent infection of HDV.