Chronic HBV infection can lead to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). HCC is one of the five major cancers in the world population. Hepatitis B virus (HBV) is the most important etiologic agent of liver cancer in the world population, particularly in areas highly prevalent for liver cancer.

Taiwan has launched the world's first universal HBV vaccination program in July 1984. The prevalence of HBV infection in vaccinated birth cohorts have been reduced remarkably to approximately one-tenth of the original prevalence. Furthermore, reduction of the HCC incidence in the vaccinated birth cohorts aged 6-14 years have been demonstrated. Recently, we have further provided evidence that the effect of HCC prevention by HBV vaccination has been extended from childhood to adolescent and gradually into early adulthood. The incidence of HCC was significantly lower among children and adolescents aged 6-19 years in the vaccinated than unvaccinated birth cohorts, showing an age- and sex-adjusted relative risk of 0.31 for the population vaccinated since birth.

Failure to prevent HCC results mostly from unsuccessful control of HBV infection by highly infectious mothers. The risk of developing HCC for vaccinated cohorts was statistically significantly associated with prenatal maternal HBsAg and HBeAg seropositivity; lack of administration of hepatitis B immunoglobulin at birth, and incomplete HBV vaccination. Future strategies to interrupt mother-to-infant transmission and to increase the global coverage rate of HBV immunization may enhance the cancer prevention effect of HBV immunization.

In conclusion, prevention of chronic HBV infection can successfully reduce the incidence of liver cancer. This is the first example of cancer preventive vaccine in human, which proves that prevention of the infection of an infectious agent can prevent its related cancer. This example has been extended to the prevention of cervical cancers, and hopefully into other infection-related cancers in the near future.

Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN01-04.