title: Analysis of carriers of hepatitis B virus from a tertiary referral hospital: does the viral load change during the natural course of infection?
abstract: This study was designed to determine the prevalence, forms of transmission, mutational profile and viral load at baseline of hepatitis B virus (HBV) carriers in Delhi. HBV surface antigen (HBsAg)-positive patients were enrolled and evaluated clinically for liver function, serological markers for hepatitis B and HBV DNA quantitation. Tests were carried out again 1 year later and the results were compared. Liver biopsy was carried out on all carriers with active viral replication. HBV DNA-positive samples were subjected to polymerase chain reaction single-stranded conformation polymorphism (PCR-SSCP) to screen mutations in the Precore, core, and the X-gene prior to sequencing analysis. Among the 100 patients examined, HBeAg was detected in 23% and 40% were HBV DNA-positive. Of the 40 HBV DNA-positive cases, 8 had precore/core mutations, [G1896A (10%), T2066A (12.5%), T2050C (10%), and G1888A (7.5%)]. No X gene mutants were detected. Reduction in viral load was higher in HBeAg-positive patients, as compared to HBeAg-negative patients, over 1 year. At follow-up, 2/8 HBV mutants corresponded with altered liver function and morphological changes suggestive of chronic hepatitis. One patient was re-designated as DNA-negative on follow-up and had wild-type virus infection with a relatively low viral load. The predominant route for HBV transmission was determined to be parenteral. Twenty percent of the HBV carriers were infected with precore and core mutant HBV. Although the clinical and biochemical profiles of these HBV carriers remained largely stable on follow-up, there was evidence of spontaneous reduction in the mean viral load over the 1-year study period.
authors.affiliation: Department of Medicine, Maulana Azad Medical College, University of Delhi, New Delhi, India.
authors.lastname: Aakanksha
authors.forename: Mohammad
authors.initials: M
authors.lastname: Asim
authors.forename: P K
authors.initials: PK
authors.lastname: Sharma
authors.forename: B C
authors.initials: BC
authors.lastname: Das
authors.forename: P
authors.initials: P
authors.lastname: Kar
mesh_terms: D000328:Adult; D000595:Amino Acid Sequence; D002353:Carrier State / Q000276:immunology / Q000821:virology*; D004279:DNA, Viral / Q000032:analysis* / Q000235:genetics / Q000276:immunology; D018450:Disease Progression; D005260:Female; D005838:Genotype; D006509:Hepatitis B / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology / Q000635:transmission / Q000821:virology; D006510:Hepatitis B Antibodies / Q000032:analysis; D006511:Hepatitis B Antigens / Q000032:analysis / Q000235:genetics* / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology; D006801:Humans; D007194:India; D008137:Longitudinal Studies; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012017:Referral and Consultation; D015534:Trans-Activators / Q000235:genetics; D019562:Viral Load; D054334:Viral Regulatory and Accessory Proteins
chemical_list: D004279:DNA, Viral; D006510:Hepatitis B Antibodies; D006511:Hepatitis B Antigens; D015534:Trans-Activators; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein