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      Global control of hepatitis B virus infection

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      The Lancet Infectious Diseases
      Elsevier BV

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          Abstract

          Worldwide about 350 million people are chronic carriers of the hepatitis B virus (HBV). The infection can cause acute and chronic liver disease including cirrhosis and hepatocellular carcinoma (HCC). Hepatocellular injuries of HBV infection are predominantly immune-mediated, and the natural history of chronic infection can be divided into three phases based on virus-host interactions-namely, immune tolerance, immune clearance, and viral integration phases. Four serotypes (adw, ayw, adr, and ayr) and seven genotypes (A to G) of HBV have been identified, and they show some distinct geographic distributions. The HBV genotypes may have clinical relevance and are currently under investigation. On the basis of disease burden and the availability of safe and effective vaccines, the WHO recommended that by the end of the 20th century hepatitis B vaccine be incorporated into routine infant and childhood immunisation programmes for all countries. The efficacy of universal immunisation has been shown in different countries, with striking reductions of the prevalence of HBV carriage in children. Most important, hepatitis B vaccination can protect children against HCC and fulminant hepatitis, as has been shown in Taiwan. Nevertheless, the implementation of worldwide vaccination against HBV requires greater effort to overcome the social and economic hurdles. Safe and effective antiviral treatments are available but are still far from ideal, a situation that, hopefully, will be improved soon. With hepatitis B immunisation, the global control of HBV infection is possible by the end of the first half of 21st century.

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          Author and article information

          Journal
          The Lancet Infectious Diseases
          The Lancet Infectious Diseases
          Elsevier BV
          14733099
          July 2002
          July 2002
          : 2
          : 7
          : 395-403
          Article
          10.1016/S1473-3099(02)00315-8
          12127351
          061b7c7d-ca88-4aed-93ad-a94ba9fbe68e
          © 2002

          https://www.elsevier.com/tdm/userlicense/1.0/

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