Update on diagnosis, management, and prevention of hepatitis B virus infection

Abstract

Acute and chronic hepatitis B virus (HBV) infection is a leading cause of liver disease worldwide. It is estimated that approximately 350 million people worldwide have chronic HBV infection and that 1 million persons die each year from HBV-related chronic liver disease. In the past decade, significant progress in the understanding of the molecular virology and pathogenesis of HBV infection has been made. In addition, effective treatment modalities have been developed for persons with chronic infection. Worldwide, prevention of HBV transmission has become a high priority. In 1992, the Global Advisory Group to the World Health Organization recommended that all countries integrate hepatitis B vaccine into national immunization programs by 1997. Currently, 80 countries have done so and several others are planning to. Many countries have reported dramatic reductions in the prevalence of chronic HBV infection among children born since the hepatitis B vaccine was introduced into infant immunization schedules. Recent reports from Taiwan indicate a reduction in the incidence of liver cancer among children as a result of widespread hepatitis B vaccination programs.

FIG. 1

Schematic diagram of hepadnavirus particles. Individual subunits containing SHBs protein only, HBs protein plus pre-S2 (MHBs), and HBs protein plus pre-S1 and pre-S2 (LHBs) are shown in intact virus, among filamensts and spheres. The virus particles contain an internal nucleocapsid (HBc) and viral genome. pol, polymerase. Reprinted from reference with permission of the publisher.

FIG. 2

Structure and organization of the HBV genome.

FIG. 3

Binding and replication of HBV. Reprinted from reference with permission of the publisher.

FIG. 4

Schematic diagram of two loops of the “a” determinant of HBs protein. The major epitope is located in the second loop between amino acids 139 and 147.

FIG. 5

T-cell response to HBV-infected hepatocytes. Inhibition of viral replication through the release of cytokines gamma interferon (IFNγ) and tumor necrosis factor alpha (TNFα) may be a key mechanism of viral clearance during acute HBV infection. CTL, cytotoxic T lymphocyte. Reprinted from reference with permission of the publisher.

FIG. 6

Characteristics of acute hepatitis B with recovery.

FIG. 7

Characteristics of progression to chronic HBV infection.

FIG. 8

Geographic distribution of chronic HBV infection.

FIG. 9

Reported cases of hepatitis B in the United States from 1975 to 1997.

FIG. 10

Liver cancer death rates in children from birth to 9 years old in Taiwan. Programs to prevent perinatal HBV transmission were initiated in 1984, and routine infant vaccination was begun in 1986. Mass campaigns to vaccinate older children and adults were conducted from 1987 to 1990. Adapted from data in reference .

FIG. 11

Countries that have integrated hepatitis B vaccine into national immunization programs, 1996. Source, Mark Kane, Global Program on Immunization, World Health Organization.