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No significant correlation exists between core promoter mutations, viral replication, and liver damage in chronic hepatitis B infection
Author(s) -
Chun Yoon Keun,
Youn Kim Jee,
Jung Woo Hong,
Myung Oh Soo,
Kang Insug,
Ha Joohun,
Kim Sung Soo
Publication year - 2000
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2000.19623
Subject(s) - hbeag , viral load , hepatitis b virus , virology , viral replication , biology , hepatitis b virus dna polymerase , hepatitis b virus pre beta , mutant , viral hepatitis , virus , mutation , hepatitis b , hbsag , gene , genetics
Hepatitis B virus (HBV) core promoter mutants have been proposed to contribute to severe liver damage by increasing viral loads, but this has not yet been clearly shown. To examine the effects of core promoter mutants on viral load and liver damage, we first developed a polymerase chain reaction (PCR)‐based semiquantitative HBV DNA detection method with a high sensitivity (able to detect as low as 10 3 molecules/mL). Then we cloned 12 predominant core promoter mutants from 41 chronic hepatitis B patients. The in vitro promoter and replication activities of these mutants were similar to those of wild‐type virus. However, viral load was highly variable, and this was dependent on individual patients rather than mutant type. In addition, there was no mutant type that showed any unique correlation with alanine transaminase (ALT) levels. Viral load was not significantly correlated with ALT level in both cross‐sectional and longitudinal studies. Quantitation of HBV levels also revealed no clear correlation between hepatitis B e antigen (HBeAg) status and viral load. Taken together, these results indicated that the replication activity of core promoter mutants has little effect on viral load, and that viral load does not correlate with the severity of liver damage or with HBeAg status.