Complete nucleotide sequences and the characteristics of two hepatitis B virus mutants causing serologically negative acute or chronic hepatitis B
Toshikazu Uchida, Kenichiro Gotoh, Toshio Shikata
Abstract
Toshikazu Uchida, Kenichiro Gotoh, Toshio Shikata
Abstract
Hepatitis B virus (HBV) DNA was amplified by the polymerase chain reaction from the sera of a patient with acute hepatitis and a patient with chronic hepatitis. Both patients were negative for serum hepatitis B surface antigen and hepatitis B core antibodies and had been previously diagnosed as non-A, non-B, non-C, non-D, non-E hepatitis. The nucleotide sequence revealed an 8-nucleotide deletion in the X-gene coding region creating a C-terminally truncated X protein, and probable mutation of the enhancer II/core promoter element. In addition, DR2 showed a T-to-C mutation at the extreme 5'-terminus. These mutations within the X-gene coding region must suppress replication and expression of HBV DNA, and this seems to be responsible for absence of serological markers despite the presence of HBV infection.
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Hepatitis B virus (HBV) DNA was amplified by the polymerase chain reaction from the sera of a patient with acute hepatitis and a patient with chronic hepatitis. Both patients were negative for serum hepatitis B surface antigen and hepatitis B core antibodies and had been previously diagnosed as non-A, non-B, non-C, non-D, non-E hepatitis. The nucleotide sequence revealed an 8-nucleotide deletion in the X-gene coding region creating a C-terminally truncated X protein, and probable mutation of the enhancer II/core promoter element. In addition, DR2 showed a T-to-C mutation at the extreme 5'-terminus. These mutations within the X-gene coding region must suppress replication and expression of HBV DNA, and this seems to be responsible for absence of serological markers despite the presence of HBV infection.
Key concepts: Virology, Hepatitis B virus DNA polymerase, Hepatitis B virus, Hepatitis B virus PRE beta, Biology, Hepadnaviridae, Gene, Mutation