When the body is infected with the hepatitis B virus, a series of immune responses occurs, and the corresponding antigens and antibodies can be detected in the serum. The hepatitis B virus is the antigen, and the body’s immune cells then produce antibodies against the hepatitis B virus. It can be seen that antigens are “invaders” and antibodies are “self-produced”. Because hepatitis B virus reproduction is different from that of germs, it first produces “parts” in the liver cells and then “assembles” these parts into a complete virus. HBsAg and HBeAg are the “parts” of hepatitis B virus, which are produced and enter the bloodstream, and are easily detected by serum immunological methods, which are easy to promote in hospitals and inexpensive. This method is easy to promote in hospitals and inexpensive, and has become a routine test for hepatitis B patients. The hepatitis B “two-and-a-half” is the most commonly used serum marker for detecting hepatitis B virus (HBV) infection in domestic hospitals, including five indicators, namely hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs), hepatitis B e antigen (HBeAg), hepatitis B e antibody (anti-HBe) and hepatitis B core antibody (anti-HBc). HBc), etc. In recent years, pre-S1 antigen with corresponding pre-S1 antibody; pre-S2 antigen with pre-S2 antibody have been isolated from hepatitis B surface antigen, commonly known as “three-and-a-half” and “four-and-a-half”. 1, HbsAg (to assist in early diagnosis, as a carrier indicator) Hepatitis B virus shell – HBsAg: Hepatitis B surface antigen is the protein shell of the hepatitis B virus, wrapped around the outermost layer of the hepatitis B virus. HBsAg alone is not contagious, but it stimulates the body’s immune function to produce anti-HBs, – once there is a large amount of anti-HBs in a person’s blood, it protects the body from getting hepatitis B again. Therefore, the main ingredient in the hepatitis B vaccine is HBsAg. HBsAg, also known as hepatitis-associated antigen (HAA), appears 2 to 8 weeks before the patient’s serum ALT rises, and the HBsAg titer gradually decreases or even disappears until the recovery period, when anti-HBs appears, but HBsAg can persist in some patients, and at this time, even if HBV has been eliminated from the body, liver cells can still keep replicating After HBV infection, most people have no clinical manifestations and are called HBsAg carriers, while a small number of people can develop acute or chronic hepatitis B, or even cirrhosis and liver cancer. The vast majority of HBV-infected people can have HBsAg in their peripheral blood, with levels ranging from 5ng to 600μg/ml, with high levels reaching over 2000μg/ml. However, a small number of HBV-infected patients have negative serum HBsAg measurements, such as fulminant hepatitis B and mutations in the S gene of HBV. The natural infection of HBV or the antibodies produced by HBsAg vaccination have no effect on the mutant strain and can cause both HBsAg and anti-HBs to appear in the patient’s serum, while hepatitis B vaccination cannot prevent infection by such mutant virus. Serum HBsAg is only a marker of HBV infection and does not reflect the presence or absence of virus replication, the degree of replication, the strength of infection and prognosis. 2, anti-HBs (hepatitis B infection is a test indicator of immunity, to determine the level of immunity of the population to the hepatitis B virus) After the recovery period of acute hepatitis B patients, with the gradual disappearance of HBsAg, anti-HBs in the serum, with protective immunity against HBV infection, at this time the surface antigen (HBsAg) has turned negative for at least 1 month, anti-HBs in 6-12 months to reach a peak, after 10mlu/m1 anti-HBs is the critical level for immunity, below this value indicates immune failure. Once a marker other than anti-HBs is present in the blood of a person who has received hepatitis B vaccination, the person should be considered to have had previous HBV infection. Generally, anti-HBs and HBsAg do not co-exist in the serum. If they are detected at the same time, they may be early in the production of anti-HBs, or belong to different subtypes of HBV infection, or be caused by the S-gene variation of HBV. 3, HbeAg (longer infectious period, is an important indicator of viral replication) Hepatitis B virus “internal parts” – HBeAg: HBeAg signifies that the hepatitis B virus is replicating and has obvious infectivity. HBeAg corresponds to anti-HBe, through treatment and self-immune regulation, HBe Ag in the patient’s blood disappears and is replaced by anti-HBe, which is called “HBeAg/anti-HBe serological conversion This is called “HBeAg/anti-HBe serological conversion”, which marks the termination of hepatitis B virus replication or only low replication, and the disappearance of infectiousness or slight infectiousness, which is a sign of “improvement”. HBeAg is a soluble component of HBcAg, and the two share about 75% of the common amino acid sequence, and appears slightly later than HBsAg in the serum, generally HBeAg positive, HBsAg is also positive. HBeAg positive indicates strong infectivity, and persistent positivity for more than 3 months has a tendency to be chronic. Sometimes a pattern of HBsAg(-), anti-HBs(+) and HBeAg(+) can be seen in the clinical laboratory, it is likely that mutations have occurred in the genetic region of the virus encoding HBsAg. 4, anti-Hbe (indicates that the disease has entered the recovery period, less infectious, acute hepatitis B indicates a good prognosis, chronic positive indicates the disease is quiescent) When the serum HBeAg turns negative, anti-HBe can appear, both positive at the same time is less common. A positive anti-HBe indicates a decrease in viral replication and is less infectious, but not non-infectious. Anti-HBe is not a protective antibody, which is different from anti-HBs. 5, HBcAb is the corresponding antibody to HBcAg It is not a protective antibody, but an indicator that the liver cells have been attacked by HBV. HBcAg, the “core component” of the hepatitis B virus: it indicates the replication of the hepatitis B virus, and its counterpart, anti-HBc, is a frequent test item. Anti-HBc is divided into two categories, one is “anti-HBclgG”, which indicates previous hepatitis B virus infection and does not disappear easily from the blood; the other is “anti-HBcIgM “, suggesting a recent infection or acute attack of hepatitis B virus, after the acute phase, anti-HBcIgM can disappear and be replaced by anti-one HBcIgG. HBcAb-IgM positivity is an indicator of acute hepatitis B virus infection and active viral replication, and is highly infectious. HBcAb-IgM positivity is also seen in chronic active hepatitis B. Whereas a positive high titer of HBcAb-IgG means ongoing infection, a low titer of HBcAb-IgG means past HBV infection and has epidemiological significance. A low titer of anti-HBc in the blood and coexisting with anti-HBs is a sign of previous infection. Such patients need to be tested for HBV DNA, and if HBV DNA is positive, occult HBV infection can be identified, and the application of immunosuppressive or cytotoxic drugs in such patients may activate the replication of HBV leading to viral destruction of liver cells. Single anti-HBc positive people should not donate blood or provide organs, etc., to avoid infecting others. At the same time, they themselves should combine work and rest, pay attention to nutrition, exercise properly, and enhance physical fitness to prevent the recurrence of hepatitis B. If there is any discomfort, they should go to hospital for examination and treatment in time. Clinical significance of two-pair pattern No. HBsAg Surface antigen Anti-HBs HBsAb Surface antibody HBeAg E antigen Anti-HBeAb E antibody Anti-HBc HBcAg Core antibody Clinical significance Occurrence rate 9 common patterns 1 – – – – – Past and present uninfected with HBV. 1-30% 2 – – – – + (1) Previous infection failed to measure anti-HBs; (2) recovered HBsAg has subsided and anti-HBs have not yet appeared; (3) asymptomatic HBsAg carrier. 5-10% 3 – – – + + (1) previous HBV infection; (2) recovery from acute HBV infection; (3) a few specimens are still infectious. (1) HBV infection has passed; (2) window period before the appearance of anti-HBs 2-10% 4 – + – – – (1) immunized with hepatitis B vaccine; (2) previous infection; (3) false positive 1-6% 5 – + – + + + recovery from acute HBV infection. 0.5-5% 6 + – – – + (1) acute HBV infection; (2) chronic HBsAg carriers; (3) weakly infectious 10-15% 7 – + – – + Pre-existing infection, still immune. hbv infection, recovery period. 5-15% 8 + – – + + (1) Acute HBV infection tends to recover; (2) Chronic HBsAg carriers; (3) Weakly infectious. That is, commonly known as “small three positive”. 5-10% 9 + – + – + Acute or chronic hepatitis B infection. Suggests HBV replication and strong infection. Commonly known as “major triplet”. 30-40% 16 rare patterns 10 + – – – – (1) Early acute HBV infection, latent acute HBV infection; (2) Chronic HBV carriers, weakly infectious. 11 + – – + – (1) Chronic HBsAg carriers with easy conversion; (2) Acute HBV infection tends to recover. 12 + – + – – Acute HBV infection in early stage or chronic carriers, highly infectious. 13 + – + + + + (1) Acute HBV infection tends to recover; (2) chronic carriers. 14 + + – – – (1) early stage of subclinical HBV infection; (2) secondary infection with different subtypes of HBV. 15 + + – – + (1) early stage of subclinical HBV infection; (2) secondary infection with different subtypes of HBV. 16 + + – + – – Subclinical or atypical infections. 17 + + – + + + Subclinical or atypical infection. 18 + + + + – + + Subclinical or atypical infection early. HBsAg immune complexes, new different subtypes of infection. 19 – – + – – (1) Atypical acute infection; (2) seen early in the infection before the appearance of anti-HBc, with low HBsAg titers and negative, or false positive. 20 – – + – + Atypical acute infection. 21 – – + + + + Acute HBV infection in the middle stage. 22 – + – + – Recovered from HBV infection. 23 – + + – – Atypical or subclinical HBV infection. 24 – + + + – + Atypical or subclinical HBV infection. 25 – – – + – – Acute HBV infection tending to recover. 7 rare patterns 26 + + + + + + + + ① a subtype of HBsAg and heterotypic anti-HBs (common); ② seroconversion from HBsAg to anti-HBs (rare). 27 – + + + – 28 – + + + + + + 29 – + + + – 30 + – + + – 31 + + + – – 32 + + + + – In conclusion, HBsAg is an antigen that appears in the serum earlier after viral infection, and HBsAg positivity is somewhat infectious, and if it does not disappear within six months, it is called chronic HBsAg carrier. HBsAg is found in saliva, sweat, breast milk, semen and vaginal secretions, and it is possible to get infected with hepatitis B virus through close contact. HBeAg positive indicates active viral replication and strong infectiousness; anti-HBc is an infectious antibody, high titer anti-HBc positive sign hepatitis B virus is replicating and infectious; anti-HBe is a non-protective antibody that appears after the e antigen is turned negative, positive indicates that viral replication is in remission, no obvious infectiousness, and the condition is recovering. Pre-S1 antigen and pre-S2 antigen are related to viral invasion of liver cells and are the first antigens to appear in the serum after human infection with hepatitis B virus, and their positivity is related to viral replication and is a sign of infectiousness; pre-S1 antibody and pre-S2 antibody positivity are signs that the virus will be cleared and have a protective effect. In addition, anti-one HBs is a protective antibody, which appears after the HBsAg turns negative, or after hepatitis B vaccination, indicating that the body has acquired immunity. Clinically, three positive HBsAg, HBeAg and anti-HBc are often referred to as “major triple-positive”. These patients have active viral replication and are highly infectious. They are mostly seen in acute hepatitis, chronic hepatitis, cirrhosis, latent phase of hepatitis B, and asymptomatic hepatitis B surface antigen carriers. The clinical manifestations are intricate and complex, with inherent characteristics in each individual. Diagnosis and treatment require a comprehensive judgment and different measures. Positive HBsAg, anti-HBe and anti-HBc are called “minor triplets”. These patients have remission of viral replication and are less infectious, and most of them are clinically indicated to be improving or recovering from the disease. Although “small three positive” patients generally do not need conventional treatment, but should not be taken lightly, pay attention to diet, rest, do not drink alcohol, regular review follow-up, to be aware of. However, clinically, “small triple-positive” patients also often have various types of chronic hepatitis and cirrhosis, which may be due to the continuous mutation of the virus in the body, the original antibodies produced can not stop the replication of the virus, or infected with other subtypes of hepatitis B virus, or intense immune disorders in the body, such patients need further in-depth comprehensive diagnosis and treatment. The measurement of hepatitis B “two-to-one” in our hospital is calculated by S/CO value, S is the absorbance (A) value of the sample to be tested, i.e. OD value – optical density of the patient’s sample, CO is the Cut off value, and the Cut off (CO) value (i.e. critical value) is calculated by the method specified in the kit used, and the result is determined according to it. The results were determined by the method specified in the kit. The so-called reactivity refers to the results of enzyme immunoassay, the S/CO value of the test sample ≥1.0, S/CO>1 is positive, HBsAg, HBsAb, HBeAg, PreS1>1 is positive, HBeAb, HBcAb<1 is positive. Because the vast majority of HBV-infected patients are only carriers, but they will also have an immune response, and get different "two-and-a-half" result patterns. Therefore, fundamentally, a positive "two-and-a-half" result reflects only HBV infection and has no causal relationship with the severity of clinical disease. When people are infected with the hepatitis B virus, they should go to the hospital as soon as possible to confirm the diagnosis, and must be under dynamic medical observation and seek help from a professional physician to jointly develop reasonable, appropriate and regular treatment measures. Patients should never take medication on their own to avoid delaying the disease and making it worse.