The X protein of hepatitis B virus (HBV) has been shown to be a trans-activator for viral and cellular genes. Amino acid sequences in X protein were found to be highly homologous to functionally essential sequences in the "Kunitz domain," characteristic of Kunitz-type serine protease inhibitors. Mutations at these sequences completely abolished trans-activation. Consequently, HBV X protein resembles a serine protease inhibitor or its analogue, and may bring about trans-activation by activating certain transcriptional factors through proteolytic cleavage alteration.
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Takada et al. (1990) studied this question.
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