HBsAg and anti-HBs HBsAg and anti-HBs are the most common and important clinical markers of hepatitis B virus, HBsAg is the outer shell of hepatitis B virus and anti-HBs is the antibody produced by the body against the surface antigen. Positive HBsAg in the serum of patients with hepatitis B virus infection is a sign of HBV infection. It is inherently antigenic and non-infectious. However, since HBsAg is often present together with HBV, it is considered one of the signs of infectiousness. However, it must be noted that HBV-DNA can reverse the integration with hepatocytes from the end of the X gene region, and the integrated S gene is strongly expressed and constantly produces HBsAg, and the integrated HBcAg genome is inhibited and does not express HBeAg and HBcAg. In this case, even though HBV has been cleared from the body, and HBsAg can still be continuously positive, theoretically, this HBsAg positive blood is not infectious. After acute HBV infection, HBsAg first appears in the serum, and can be positive throughout the acute period, and can titer down or turn negative during the recovery period. If HBsAg continues to be positive for more than six months, it is called chronic HBsAg carrier (asymptomatic HBsAg carrier) and can continue to be positive for several years. It is generally believed that HBsAg titer is not proportional to the degree of disease. With normal liver function and high HBsAg titers, the liver may be free of obvious lesions, and if HBsAg is negative and DNAp is negative, it means no significant infectiousness. Conversely, abnormal liver function, HBsAg titer is not high, the liver can have obvious lesions, such as some patients with cirrhosis and liver cancer are HBsAg negative or low titer. Asymptomatic HBsAg carriers or chronic active hepatitis B can have the same HBsAg titer changes cannot represent the severity of the disease, so decomposition of this can not be the change in HBsAg titer as an indicator of the severity of the disease. The mechanism of HBsAg in hepatocyte plasma confirmed by immunoelectron microscopy and immunofluorescence, but HBsAg negative in serum, has not been exactly explained. One of the known reasons for this is that the RIA test, which has a sensitivity of 10-5, is not yet able to measure the minimum amount of infection (10-7), so there is a 10% false negative, so the judgment of HBsAg, positive has diagnostic significance, and negative cannot exclude HBV infection. In recent years, it has been found that HBV markers in serum are negative, but HBV-DNA is detected in leukocytes or hepatocytes, indicating that determining or excluding HBV infection cannot be based on HBsAg positivity alone, but should be combined with other markers. There are 10 subtypes of HBsAg, and incomplete cross-immunity exists among the subtypes. Recent studies with subtype monoclonal antibodies have shown that d and y, w and r determinants can exist simultaneously on the same viral antigen particle, forming adwr, aywr, adyw and adyr complex subtypes. The mechanism is (i) dual infection with different subtypes of virus; (ii) point mutations in some HBV-DNA after infection with a single subtype of virus. Clinical manifestations of the disease are recurrent and liver damage is more severe, thus some HBV-infected patients have both HBsAg-positive and anti-HBs-positive sera. Anti-HBs is a protective antibody produced after HBV infection or hepatitis B vaccination. Anti-HBs appears 6 to 23 weeks after the initial HBV infection, about 20% appear early in the infection, and anti-HBs appears several months to 1 year after the disappearance of HBsAg in the recovery period. Positive anti-HBs indicates that immunity has been acquired. The potency of anti-HBs is measured quantitatively and anti-HBs potency ≥ IUml is considered to indicate protection. HBsAg and anti-HBs are usually not present at the same time. They can be present in blood and various body fluids.