To study the replicative efficiency and pathogenicity of hepatitis B virus
precore variant (A1896), anti-hepatitis B virus e antigen (HBe) titre was s
tudied in naturally occurring wild-type virus infection, A1896 variant infe
ction and dual infection. Higher titre of anti-HBe was found in patients wi
th no virus replication and in patients coinfected with the wild-type virus
and A1896 variant, which suggest that anti-HBe may either act as an inhibi
tor of virus replication or as selective pressure for the A1896 variant. Th
ree site-directed mutants were constructed in the duck hepatitis B virus (D
HBV) precore region. A frame shift in the encapsidation signal region aboli
shed replication of DHBV; mutation in the initiation codon of the precore a
nd mutation to generate a termination codon at the distal region of the pre
core resulted in decreased replication in the duck model. More significant
pathological changes were found in the liver tissues of ducks infected with
the mutant which mimicked the HBV A1896 variant.