Abstract
Results: Endogenous expression of L-, S-, coreor HBe-protein did not result in a significant interference with the subsequent infection with HDV. However, expression of L-protein drastically reduced HBV infection efficacy. In contrast, S-protein expression had only marginal effect on both viruses. By mutation analysis on the preS-domain, we found that deletions in the capsid binding region restored the susceptibility to HBV infection. Conclusions: The presence of preS-domain of L-protein specifically interferes with HBV superinfection through its capsid binding domain. This is not due to a regulation of virus receptor since the HDV infection remains unaffected. We hypothesize that the released incoming nucleocapsid might be hindered from trafficking to the nucleus by pre-existing L-protein. Thus, L-protein might act as a regulator of intracellular nucleocapsid trafficking in order to discriminate between HDV and HBV superinfection.
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