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Quantitative DNA analysis of low‐level hepatitis B viremia in two patients with serologically negative chronic hepatitis B
Author(s) -
Saito Takafumi,
Shinzawa Haruhide,
Uchida Toshikazu,
Kawamata Osamu,
Honma Sayaka,
Watanabe Hisayoshi,
Shao Li,
Saito Koji,
Togashi Hitoshi,
Takahashi Tsuneo
Publication year - 1999
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199908)58:4<325::aid-jmv2>3.0.co;2-l
Subject(s) - virology , hbsag , viremia , hepatitis b virus , hepatitis b virus dna polymerase , biology , hepatitis b virus pre beta , hepatitis b , polymerase chain reaction , hepadnaviridae , orthohepadnavirus , virus , microbiology and biotechnology , gene , genetics
Low‐level viremia due to hepatitis B virus (HBV) was demonstrated in the sera of two patients diagnosed previously as having non‐B, non‐C chronic hepatitis. Both patients had a “silent” HBV infection, because they were negative for both hepatitis B surface antigen (HBsAg) and anti‐hepatitis B core antibody. The TaqMan chemistry polymerase chain reaction (PCR) amplified the HBV DNA, enabling quantitation of the virus in their sera. Their serum HBV DNA concentrations were low: the amount of each HBV S or X gene amplified showed there were approximately 10 3 copies/ml and HBV DNA was detected occasionally during clinical follow‐up. Positive HBsAg staining in liver tissues was demonstrated by an immunoperoxidase technique. Vertical transmission of silent HBV from one patient to her daughter was confirmed. Direct nucleotide sequencing of the amplified HBV X region revealed several mutations, suggesting reduced viral replication. One patient had a T‐to‐C mutation at the extreme 5′‐terminus of the direct repeat 2 region and the other exhibited a coexisting X region with a 155‐nucleotide deletion. These findings suggest that HBV replication is suppressed considerably in patients with silent hepatitis B. J. Med. Virol. 58:325–331, 1999. © 1999 Wiley‐Liss, Inc.