Pathogenesis
Hepatitis B virus is dangerous because it attacks the liver, thus inhibiting the functions of this vital organ. The virus causes persistent infection, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, and immune complex disease.
HBV infection in itself does not lead to the death of infected hepatocytes. HBV in a non-cytolytic infection. Liver damage however, arises from cytolytic effects of the immune system's cytotoxic T lymphocytes (CTL) which attempt to clear infection by killing infected cells. The strength of the CTL response has been noted to determine the course of the infection. For example, a vigorous CTL response results in clearance and recovery, although often with an episode of jaundice. A weak response results in few symptoms and chronic infection (and hence higher susceptibility for hepatocellular carcinoma).
The younger a person is when she becomes infected with HBV, the more likely she is to be asymptomatic and become a chronic carrier of the disease. Babies born to infected mothers are at very high risk of to becoming carriers and developing liver pathology.
Vertical is thus one common way that HBV is transmitted, along with transmission through sexual intercourse and mixing of blood products. Vertical transmission can be prevented by administering vaccine the same day of birth. Different modes of transmission are more prevalent in certain areas of the world and among certain high-risk groups, yet all areas of the world see HBV transmission through all of these avenues. About 90% of adults who acquire HBV recover from it completely and become immune to the virus. The other 10% of cases are the people who become chronic carriers.
Source:
Strauss, James and Ellen. Viruses and Human Disease. Academic Press, San Francisco: © 2002.
Farber E, Phillips FT, and Kaufman WA (eds). Pathogenesis of Liver Disease. Los Angeles: Williams and Wilkins, 1987.
Mahoney, Franics J. and Mark Kane. "Hepatitis B Vaccine" Chapter 10 in Vaccines,
3rd ed. Stanley A. Plotnick and Walter A. Orenstein, eds. W.B. Saunders Company;
Philadelphia, 1999 (159-82).