Thence the Committee decided our next task of high priority is to produce the practical guidelines for hepatitis B, also a significant burden to the health care system. Here the Committee has launched the Guidelines for the Management of Hepatitis B Virus Infection. As with hepatitis C virus, this is a field that changes rapidly with the accumulation of new evidence, accompanied by changes in the level of evidence, so we have elected not to show evidence levels. We plan to update these guidelines at appropriate intervals, as new evidence comes to hand.

It is estimated that there are 400 million patients of persistent hepatitis B virus (HBV) infection in the world.[1] In Japan, the HBV infection rate is around 1%. HBV infection at birth or during infancy leads to persistent infection in over 90% of cases. Approximately 90% of these undergo seroconversion from HBe antigen (HBeAg) Selleckchem PD98059 positive at the initial stage to anti-HBe antibody Gefitinib price positive and become inactive carriers, and in virtually all cases the condition effectively stabilizes. But in the remaining 10% the virus remains active, leading to chronic hepatitis, and in around 2% of cases annually, there is further progression to liver cirrhosis, with potential for hepatocellular carcinoma (HCC) and liver failure.[2-4] Clinical research on HBV dates back to the discovery of the Australia antigen (later renamed HBs antigen; HBsAg) by Blumberg et al.

in 1964. Prince et al. and Okouchi et al. subsequently reported a link between the Australia antigen and hepatitis. And there have been various other discoveries demonstrating that MCE公司 the existence of an asymptomatic carrier, who does not develop hepatitis following HBV infection and indicating HBV as a cause of chronic liver diseases. The base form of HBV, known as the Dane particle, was discovered in 1970, followed by the identification of HBeAg in 1972. In 1979, the whole HBV genome was successfully cloned from virus particles,

enabling measurement of the virus gene (HBV DNA) for the first time. In Japan, screening for the HBsAg was introduced at blood centers in 1972. 1986 was the year of the introduction of an anti-HBV vaccine and immunoglobulin for newborns designed to prevent vertical (mother-to-child) infection. This was highly effective in arresting the development of new HBV carriers through vertical infection, causing a marked decline in HBsAg positive rates among juveniles. The incidence of acute hepatitis caused by HBV infection, however, has not declined, mainly as a result of horizontal transmission associated with sexual activity. In recent years, there has been an increase in infection rates for the HBV genotype A, which frequently causes persistent infection.[5] HBV in itself is considered to have little or no cytotoxicity. Hepatocellular damages are generally caused by cellular immunity associated with cytotoxic T cells, which represent the host’s immune response attacking HBV infected cells.