| Approximately 350 million people are chronic carriers of HBV in wold. Of these, only 1% to 2% will annually spontaneously clear hepatitis B surface antifen (HBsAg). Ultimately, more than half of HBsAg-positive patients will die of hepatocellular carcinoma or liver failure. Viral and host factors, such as age, immunosuppression, and sex contribute to the patient outcome.In Asian countries, by far the most patients with chronic HBV infection have acquired the infection perinatally from carrier mothers positive for hepatitis B e antigen (HBeAg). During the first few to several decades of life, they are positive for HBeAg, but some of them seroconvert to antibody to HBeAg (anti-HBe) accompanied by elevation in alanine transaminase (ALT) levels, whereas others continue to have HBeAg with or without elevated ALT. In addition, there are patients in whom elevated ALT levels persist even after they have seroconverted to anti-HBe. The molecular biological basis for HBeAg-positive or negative phenotype of HBV has been studied in depth. Many investigators have reported the association of mutations in the HBV genome with HBeAg as well as viral replication. The G toA mutation at nucleotide (nt) 1896 in the precore (PreC) region (A 1896), converting codon 28 for tryptophan to a stop codon, is associated with the loss of HBeAg. The double mutation in the basic core promoter (BCP), A to T mutation at nt!762 and G to A mutation at nt 1764 (T1762/A1764) is associate with reduced synthesis of HBeAg by means of suppressing the transcription of precore mRNA. Despite their roles in the synthesis of HBeAg, clinical and virological significance of PreC and BCP mutations are not yet fully understood.Seven genotypes of HBV are recognized that are distinguished by difference of more than 8% in the entire mucleotide sequence of approximately 3,200 nt, and they are designated by capital letters from A to G. HBV genotypes have distinct geographical distributions. Overall, genotypes B and C are frequent in Asia, whereas genotypes A and D prevail in Western countries. Genotype E is restricted to Africa, and genotype F prevails in Central America. Genotype G was added to the alphabet list very recently, and its distributaion is yet to be determined. Although serological and genotypic classifications of HBV have been well recognized, the clinical significance of HBV genotypes, in terms of clinical outcomes and therapeutic response to antiviral therapy in patients with chronic HBV infections, has remained largely unknown until recently.During the HBV infection the viral load varies greatly during the different phases, and correlates strongly with the extent of hepatitis and the disease outcome. Dramatic changes inviral load also occur in response to treatment with anti-viral agents such as lamivudine. Therefore in the clinical setting, detection assays are required which can measure HBV load quantitatively and sensitively over a wide range of virion concentrations. Quantitative measurements of HBV DNA are currently performed using the polymerase chain reaction (PCR), transcription-mediated amplification (TMA), or signal amplification rsing branched-DNA. Although molecular amplification assays are highly sensitive, their cost, complexity and the risk of contamination render them unsuitable for routine use in the clinical diagnostic laboratory outside the research setting. Recently, two chemiluminescence enzyme immunoassays (CLEIA) were developed specific for HBV were developed. One is an HBV core-related antigen (HBcrAg) assay that measures the serum levels of hepatitis B e antigen (HBeAg) and hepatitis B core antigen (HBcAg) simultaneously using monoclonal antibodies, and the other is an assay that measures the serum level of HBcAg. Although assessments of clinical performance relating to the HBcAg and HBcrAg assay have already been reported in Japanese patients, evaluation of these two antigen assays was not performed in patients with HBV genotype B. Part one: The study of prevalence of hepatitis B Virus (HBV) genotype in patients with chr...
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