How does chronic hepatitis B virus carriage occur? The vast majority of chronic hepatitis B carriers were infected as children, either from their mothers, family members, or from social transmission. The immune system in children is not fully developed and is not easily cleared after infection with hepatitis B. Once this state occurs, it will persist for a long period of time, which is called “immune tolerance” in medical terms, resulting in chronic carriage. The chronic carriage rate has been reduced from 10% to 1% after the implementation of the comprehensive pediatric vaccine immunization program, but a small number of infants and children are still infected. Infection occurs mainly in newborns of e antigen (HBeAg)-positive mothers for a variety of reasons: inadequate doses of our hepatitis B vaccine; failure to combine hepatitis B immunoglobulin; failure of even standardized prophylactic regimens if the mother’s serum viral levels are high, and these pregnant women are best advised to consult a specialist; few newborns can be infected in utero; and a few newborns do not respond to the hepatitis B vaccine. A small number of newborns do not respond to the hepatitis B vaccine. Hepatitis B virus causes a chronic, nonpathogenic infection of the hepatocytes. Hepatocytes can continue to secrete virus, infecting the vast majority of liver cells. The hepatocytes are long-lived, so the virus can continue to infect for long years. It may take several generations to control the hepatitis B virus epidemic. Can I be infected with the hepatitis B virus without developing the disease? The hepatitis B virus replicates mainly in liver cells, but does not interfere much with cellular metabolism, so it does not directly cause cytopathy. The hepatitis B virus in chronic hepatitis B carriers seems to “coexist” with the immune system: the virus does not cause inflammatory damage to liver cells, and most infected people remain healthy; the immune system of infected people also tolerates the replication of the virus in liver cells. This is the state of immune tolerance; if it does not “coexist”, the immune attack on the virus in the liver cells will also cause damage to the liver cells. It is understandable why e antigen positive (so-called “major triple positive”) carriers have varying degrees of immune tolerance, i.e., they suppress immune attack on the hepatitis B virus, neither clearing the virus nor causing hepatocellular lesions, and have high serum virus levels without hepatitis. What is the difference between e antigen-positive and e antigen-negative carriers? As immune tolerance declines with age, the level of serum viral nucleic acid (HBV DNA) gradually decreases to a certain level (≈1×104 copies/mL), and the titer of e antigen decreases and becomes negative with it. Thus, the detection rate of e antigen decreases with age: nearly 90% in infancy, about 50% in adolescence, about 25% in young adulthood, and less than 10% after 45 years of age. HBeAg(+) stage: the high infection status is quite stable in a certain period of time, HBeAg and HBV DNA levels decrease very slowly, serum transaminases continue to be normal, and there are no obvious lesions in liver histology. The HBeAg(+) period is very long, with only 5-10% of carriers turning HBeAg negative each year, and most people need to be 40 years old or older. All chronic hepatitis B carriers are converted from HBeAg(+) to HBeAg(-).