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• W139805017 abstract "Despite unceasing efforts of the medical community, hepatitis B remains, besideshepatitis C, the most serious type of viral hepatitis and one of the major problems ofglobal public health. According to the latest World Health Organization fact sheets(2000), of the 2 billion people who have been infected with the hepatitis B virus (HBV),more than 350 million have chronic infections. These chronically infected persons areat high risk of death from cirrhosis of the liver and liver cancer, diseases that kill about 1million persons each year (WHO, 2000).The prevalence of HBV varies tremendously in different part of the world, with a muchhigher incidence in the Eastern than in the Western Hemisphere (WHO, 2001). Highprevalence areas have been identified in Southeast Asia, China and Africa (reviewed byLee, 1997). About 100 million carriers, making up 75% of the world’s HBV carriersliving in Asia, are from China (Tandon and Tandon, 1997). In Malaysia, voluntarytesting carried out on 17 048 healthy volunteers indicated a HBsAg seropositivity of5.24% (Merican et al., 2000).xxvHBV belongs to the Orthohepadnavirus genus of the Hepadnaviridae family, which isrelated to the large order of Retroid viruses (Kann and Gerlich, 1998). Within a size ofonly about 3.2 kb, its compact, partially double-stranded DNA genome is extremelysmall, bearing four highly overlapping open reading frames (ORFs), which encode atleast seven proteins (Kann and Gerlich, 1998; Nassal, 1999; Seeger and Mason, 2000).Due to the use of a viral RNA-dependent polymerase without proofreading function,HBV has a higher mutational rate than other DNA viruses (Blum1995; Petzold et al.,1999). Thus, it is generally assumed that this reverse transcription step accounts for themajority of point mutations and deletions or insertions that can be observed in the HBVgenome.There are 2 major types of mutations in HBV. Firstly, there are genotype-specificmutations that allow the distinction of currently eight genotypes (A-H) (Norder et al.,1993; Stuyver et al., 2000; Arauz-Ruiz et al., 2002). These genotypes clustergeographically. Genotype A seems to represent the main European inland strain;genotype B and C, the Asian strain; genotype D, the Mediterranean basin strain;genotype E, the African strain; and genotype F, the New World strain (Norder et al., 1994;Magnius and Norder, 1995; Kidd Ljunggren, 1996). Genotype G was identified inFrance and United States (Stuyver et al., 2000) and genotype H was recently encounteredin Nicaragua, Mexico and California (Arauz-Ruiz et al., 2002).xxviThe second type of HBV variability concerns mutations that emerge in an individualduring chronic infection. Several specific mutations of this type have been identified bya large number of longitudinal as well as cross-sectional studies conducted during thepast decade (reviewed in Gunther et al., 1999). Most of the corresponding variantsaccumulate during infection and persist as a dominant population until the late phase.These mutants are clinically important. It is learned that the presence or emergence ofspecific mutations is associated with particular stages of chronic infections (Gunther et al.,1999).In general, the enhancer II/core promoter and precore stop codon mutants appear to beassociated with disease severity and progression (Lindh et al., 1999; Scaglioni et al.,1997; Pult et al., 1997; Takahashi et al., 1999). Mutations in the core antigen contributestrongly to immune escape at the T helper and cytotoxic T lymphocyte (CTL) level(Wakita et al., 1991; Chisari and Ferrari, 1995). Recent reports also revealed thatmutations at basal core promoter (BCP) and precore/core (preC/C) mutations mayinfluence the response rate to interferon-alpha (IFN-α) therapy (Fattovich et al., 1995;Zhang et al., 1996; Erhardt et al., 2000). Surface antigen mutants allow for escape fromhumoral immune responses and reduce the effectiveness of diagnostic tests andvaccination (Waters et al., 1992; Karthigesu et al., 1994; Carman et al., 1995,; Wallaceand Carman, 1997; Hsu et al., 1999a).xxviiHBV is a typical non-cytopathic virus that can induce tissue damage of variable severityby stimulating a protective immune response that can simultaneously cause damage andprotection, by resolving intracellular virus through the destruction of virus infected cells(Ferrari et al., 2003). Therefore, immune elimination of infected cells can lead to thetermination of infection when it is efficient, or to a persistent necroinflammatory diseasewhen it is not.Destruction of infected cells, however, is not the only mechanism implicated in theelimination of intracellular virus, as demonstrated by studies carried out in humanhepatitis B showing the importance of cytokine-mediated, non-cytolytic mechanisms ofantiviral protection. The first experimental evidence in favour of such mechanismsderives from studies performed in the transgenic mouse model (Guidotti and Ferrari,2001). These studies showed that single stranded and relaxed circular double strandedHBV DNA replicative intermediates can be eliminated from the cytoplasm of HBVtransgenic hepatocytes as a result of the antiviral effect of the interferon-gamma (IFN-γ)and tumour necrosis factor-alpha (TNF-α) released within the transgenic liver primarilyby infiltrating HBV-specific CD8+ cells (Guidotti et al., 1996; Heise et al., 1999b) butalso CD4+ T cells (Franco et al., 1997).Although the existence of genotypes is known for a long period of time, only veryrecently an association of genotype and clinical outcome was proposed (Kao et al., 2000a;Lindh et al., 1999). Recently, HBV genotypes have been partially clarified asxxviiiinfluencing the clinical manifestation of chronic liver disease in hosts. A higherdisease-inducing capability of genotype C than genotype B has been observed in Asia(Orito et al., 2001a; Kao et al., 2000a; Lindh et al., 1999). Several studies, mostly fromTaiwan and Japan, have shown that HBV genotype C is associated with the developmentof hepatocellular carcinoma (HCC) (Kao et al., 2000a; Ding et al., 2001; Fujie et al.,2001) and has a lower response rate to interferon therapy as compared to genotype B(Kao et al., 2000b). As for other HBV genotypes, most patients in Europe with genotypeA have chronic hepatitis, whereas most patients with genotype D have acute hepatitis(Mayerat et al., 1999) and may predict the occurrence of HCC in young Indian patients(Thakur et al., 2002).The genotype-related differences in HBV pathogenesis have been associated with theHBeAg/anti-HBe status. In the natural course of chronic HBV infection, earlyHBeAg/anti-HBe seroconversion usually associated with the cessation of virusreplication and thus a favourable outcome (Chen, 1993). In contrast, late seroconversionof HBeAg after multiple episodes of reactivation and remission may accelerate theprogression of chronic hepatitis B and thus have a poor clinical outcome (Perillo, 2001).Reports have revealed that the prevalence of HBeAg is more common in HBV genotypeC than B. The reverse held true for the prevalence of anti-HBe, in that it is less commonin genotype C than B (Ding et al., 2002; Chu et al., 2002; Kao et al., 2002; Orito et al.,2001a; Kobayashi et al., 2002; Yuen et al., 2003; Akuta et al., 2003).xxixTaken together, these data from different parts of the world have lent strong support topossible pathogenic differences among HBV variants. At present, those findings havebeen reported only in a few Asian countries. Moreover, the molecular virologicmechanisms that contribute to these clinical differences among HBV genotypes remain tobe explored. The major limitation of previous studies is the lack of simple and efficientgenotyping methods. Genotyping of viruses by sequencing and subsequent homologycomparison or phylogenetic tree analysis is tedious and labour intensive and, therefore,not practical for diagnostic purposes. With the recent advances in molecular techniques,several novel genotyping methods, including polymerase chain reaction-restrictionfragment length polymorphism (PCR-RFLP) (Lindh et al., 1997; Mizokami et al., 1999),PCR with type-specific primers (Naito et al., 2001), commercial hybridization assay(Hou et al., 2001) and serologic genotyping assay (Usuda et al., 1999) have beenintroduced.In Malaysia, where the incidence rate of HBV was 12.19 per 100,000 population in 2001(Ministry of Health Malaysia, 2001), limited information on the molecular biology of theHBV is available. The prevalence of HBV genotypes and the clinical relevance of HBVvariants have not been discussed. The studies from other areas may not apply worldwidebecause the HBV strains in various parts of the world are different, and thus the clinicaloutcome and the mechanisms responsible may be different in this country. Thisprovided a strong motivation to investigate the molecular variants of HBV in ourpopulation and the immune response evoked by these HBV variants." @default.
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• W139805017 title "Molecular and Cellular Studies of Human Hepatitis B Virus Variants" @default.
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