Base-pair Alterations in the Epsilon-lower Stem due to a Novel Double Substitution in the Precore Gene of HBV-e Negative Variant were Recovered by Secondary Mutations

[1]  T. Su,et al.  The encapsidation signal of hepatitis B virus facilitates preC AUG recognition resulting in inefficient translation of the downstream genes. , 1999, The Journal of general virology.

[2]  A. Dhillon,et al.  Hepatitis B virus carriers without precore mutations in hepatitis B e antigen‐negative stage show more severe liver damage , 1996, Hepatology.

[3]  A. Kidd,et al.  A revised secondary structure model for the 3'-end of hepatitis B virus pregenomic RNA. , 1996, Nucleic acids research.

[4]  A. Faruqi,et al.  The mechanism of natural occurrence of two closely linked HBV precore predominant mutations. , 1995, Virology.

[5]  U. Akarca,et al.  Predictive value of precore hepatitis B virus mutations in spontaneous and interferon‐induced hepatitis B e antigen clearance , 1995, Hepatology.

[6]  S. Tong,et al.  Evidence for a base-paired region of hepatitis B virus pregenome encapsidation signal which influences the patterns of precore mutations abolishing HBe protein expression , 1993, Journal of virology.

[7]  J. Pollack,et al.  An RNA stem-loop structure directs hepatitis B virus genomic RNA encapsidation , 1993, Journal of virology.

[8]  S. Mishiro,et al.  Fulminant hepatitis related to transmission of hepatitis B variants with precore mutations between spouses , 1992, Hepatology.

[9]  J. Wands,et al.  Persistence of hepatitis B viral DNA after serological recovery from hepatitis B virus infection , 1991, Hepatology.

[10]  C. Guguen-Guillouzo,et al.  In vitro replication competence of a cloned hepatitis B virus variant with a nonsense mutation in the distal pre-C region. , 1991, Virology.

[11]  C. Trépo,et al.  Active hepatitis B virus replication in the presence of anti-HBe is associated with viral variants containing an inactive pre-C region. , 1990, Virology.

[12]  F Tsuda,et al.  Hepatitis B viruses with precore region defects prevail in persistently infected hosts along with seroconversion to the antibody against e antigen , 1990, Journal of virology.

[13]  F. Callea,et al.  Chronic hepatitis in HBsAg carriers with serum HBV-DNA and anti-HBe. , 1986, Gastroenterology.