Cases reported "Hepatitis B, Chronic"

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1/5. Antiviral treatment for human immunodeficiency virus patients co-infected with hepatitis b virus: combined effect for both infections, an obtainable goal?

    A large percentage of human immunodeficiency virus (hiv) patients have serological evidence of a past or present hepatitis b virus infection (HBV). Long-term survival is increasing for hiv patients because of highly active antiretroviral therapy. Therefore, the chronic hepatitis B infection may become an important determinant of disease outcome in these co-infected patients. We describe two hiv/HBV co-infected patients who were treated with extended antiviral therapy, initially indicated for the hiv infection. lamivudine, a suppressor of viral replication in both infections, was one of these antiviral drugs. One patient showed a severe rebound of the HBV after withdrawal of lamivudine, the other patient developed a mutant hepatitis b virus after 18 months of treatment. This mutation was exclusively induced by lamivudine. These patients show that, with improved hiv-related survival, the HBV infection should be monitored carefully, thereby enabling the physician to interfere with therapy when necessary.
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2/5. A novel stop codon mutation in HBsAg gene identified in a hepatitis b virus strain associated with cryptogenic cirrhosis.

    AIM: HBsAg is the most important serological marker for acute or chronic hepatitis B. Nevertheless, there were reports of HBsAg-negative infection caused by hepatitis b virus in recent years. We had a patient with crytogenic cirrhosis who was negative for HBsAg, positive for anti-HBs and HBeAg. This paper was to explore the pathogenic and molecular basis of the unusual serological pattern. methods: HBV serologic markers were qualitatively and quantitatively determined. HBV dna in serum was qualitatively tested using routine polymerase chain reaction(PCR), and the viral level was determined with real-time fluorescence quantitative PCR. HBsAg gene was amplified and cloned. Four clones were sequenced. The new genomic sequences were compared with GenBank on the dna level as well as the protein level. RESULTS: The qualitative results of serological markers were HBsAg(-), anti-HBs( ), HBeAg( ), anti-HBe(-) and anti-HBc( ). The quantitative results of serological marker were HBsAg (S/N): 0.77 (cut off of S/N: >=2.00), HBeAg (S/N): 56.43 (cut off S/N: >=2.10), anti-HBc (S/C(0)): 2.03 (cut off of S/C(0): <=1.00). The viral level was as high as 1.54 x 10(9) copies/ml. Sequencing of the HBsAg gene clones revealed a unique point mutation at nucleotide 336 (C to A), which resulted in a novel stop codon at aa 61. The novel HBsAg gene stop mutation had not been described. CONCLUSION: The lack of detection of HBsAg in the presence of high viral levels of replication may be caused by the existence of viral genomes harboring point mutations which resulted in stop codon upstream of the "a" determinant in HBsAg gene.
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3/5. Transmission of G145R mutant of HBV to an unrelated contact.

    Household contacts of HBV-related chronic liver disease patients constitute a high-risk group for acquisition of HBV infection. Some of the HBsAg mutants are associated with liver disease and some are reported to be transmitted vertically. There is limited information on the horizontal transmission of Gly 145 Arg (G145R) mutant to related contacts. Its possible transmission to an unrelated third degree contact is reported in the present study. An HBV related chronic liver disease patient; the index patient, and his 11 household contacts were studied. This included four 1 degrees, three 2 degrees, one 3 degrees, and a sexual contact. Surface gene sequencing including the "a" determinant region was carried out in HBV dna ve subjects. The sequences were aligned and compared for the homology. HBV dna was found to be positive in one 1 degrees, three 2 degrees, and one 3 degrees contact, besides the index patient. Histopathological studies revealed evidence of chronic hepatitis in all these contacts. Mutation T118V was present in all the six subjects. Mutant G145R along with T118V and T143M was identified in three subjects who included one 1 degrees, one 2 degrees, and one 3 degrees contact. Presence of T118V and T143M mutations along with G145R mutation in these subjects provides an indirect evidence for the possible horizontal transmission of G145R HBV variant to a 3 degrees unrelated contact. Of these three contacts with G145R mutation, only one 1 degrees contact was found to be HBsAg-ve. The data also reaffirms the earlier finding of HBsAg positivity in presence of G145R mutation of the S-gene. HBV exists as quasi-species and mixed population in subjects with chronic HBV infection.
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4/5. Overlapping gene mutations of hepatitis b virus in a chronic hepatitis B patient with hepatitis B surface antigen loss during lamivudine therapy.

    Disappearance of hepatitis b surface antigens (HBsAg) in chronic hepatitis B usually indicates clearance of hepatitis b virus (HBV) infection. However, false HBsAg negativity with mutations in pre-S2 and 'a' determinant has been reported. It is also known that YMDD mutations decrease the production of HBV and escape detection of serum HBsAg. Here, we report overlapping gene mutations in a patient with HBsAg loss during the lamivudine therapy. After 36 months of lamivudine therapy in a 44-yrold Korean chronic hepatitis B patient, serum HBsAg turned negative while HBV dna remained positive by a dna probe method. Nucleotide sequence of serum HBV dna was compared with the HBV genotype C subtype adr registered in NCBI AF 286594. Deletion of nucleotides 23 to 55 (amino acids 12 to 22) was identified in the pre-S2 region. Sequencing of the 'a' determinant revealed amino acid substitutions as I126S, T131N, M133T, and S136Y. methionine of rtM204 in the P gene was substituted for isoleucine indicating YIDD mutation (rtM204I). We identified a HBV mutant composed of pre-S2 deletions and 'a' determinant substitutions with YMDD mutation. Our result suggests that false HBsAg negativity can be induced by combination of overlapping gene mutations during the lamivudine therapy.
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5/5. Emergence of an S gene mutant during thymosin alpha1 therapy in a patient with chronic hepatitis B.

    The presence of a hepatitis b virus S gene mutant was investigated in a patient being treated with thymosin alpha1. He was seropositive for hepatitis B e antigen throughout therapy but was intermittently seronegative for hepatitis B surface antigen (HBsAg) by an RIA. sequence analysis revealed an S gene mutant in HBsAg-seronegative serum with two consecutive amino acid substitutions: threonine115-to-isoleucine and threonine116-to-asparagine, whereas no amino acid substitution or deletion was found in the pre-S region. A site-directed mutagenesis experiment confirmed that these mutations were responsible for the failure to detect HBsAg. In summary, an S gene mutant was identified in an HBsAg-seronegative patient. The mutations were located outside the putative "a" determinant. The emergence of an S gene mutant during thymosin alpha1 treatment suggests that enhanced host immunity against HBsAg may play a role in its antiviral activity.
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