This guideline is intended to help physicians make rational decisions in the diagnosis and prevention of chronic hepatitis B. It is not a mandatory standard and cannot include or address all issues in the diagnosis and treatment of chronic hepatitis B. Therefore, when faced with a particular patient, clinicians should develop a comprehensive and reasonable treatment plan based on their professional knowledge, clinical experience, and available medical resources, with full knowledge of the best clinical evidence about the disease and careful consideration of the patient’s specific condition and his or her wishes. We will continue to update and improve this guideline in accordance with relevant advances at home and abroad. I. Pathogenesis. Hepatitis B virus (HBV) belongs to the family of hepadnaviridae, with a genome length of about 3.2 kb and a part of double-stranded circular DNA. HBV has a strong resistance, but HBV can be inactivated by 65℃ for 10 h, boiling for 10 min or high pressure steam. ethylene oxide, glutaraldehyde, peroxyacetic acid and iodine volt are also effective in inactivating HBV. After HBV invades hepatocytes, part of the double-stranded cyclic HBV DNA is used in the nucleus to extend the positive chain with negative-stranded DNA as a template to repair the gap area in the positive chain, forming covalent closed-loop DNA (cccDNA); then cccDNA is used as a template to transcribe into several mRNAs of different lengths, which are used as pregenomic RNA and encode various antigens of HBV. (The cccDNA has a long half-life and is difficult to completely remove from the body. HBV has been found to have 9 genotypes from A to I. In China, the C and B genotypes are predominant. HBV genotype is associated with disease progression and the effect of interferon alpha therapy. Compared with C genotype infected patients, B genotype infected patients show HBeAg serological conversion earlier and progress less to chronic hepatitis, cirrhosis and primary hepatocellular carcinoma; and the response rate of HBeAg positive patients to interferon alpha therapy is higher than that of C genotype; A genotype patients are higher than that of D genotype. Second, epidemiology. HBV infection is endemic worldwide, but the prevalence intensity of HBV infection varies greatly from region to region. According to the World Health Organization, about 2 billion people worldwide have been infected with HBV, 350 million of them are chronic HBV infected, and about 1 million people die each year from liver failure, cirrhosis and primary hepatocellular carcinoma (HCC) caused by HBV infection. In 2006, the National Hepatitis B Epidemiological Survey showed that the HBsAg carriage rate of the general population aged 1-59 in China was 7.18%, and the HBsAg in children under 5 years old was only 0.96%. It is projected that there are about 93 million people with chronic HBV infection in China, including about 20 million cases of chronic hepatitis B patients. HBV is a blood-borne disease and is mainly transmitted via blood (e.g., unsafe injections, etc.), mother-to-child and sexual contact [14]. Due to the implementation of strict HBsAg screening for blood donors, HBV infection caused by blood transfusion or blood products has been less frequent; transmission through broken skin and mucous membranes is mainly due to the use of medical devices that are not strictly sterilized, invasive diagnostic and surgical operations, unsafe injections, especially drug injections; others such as pedicure, tattoo, earring piercing, accidental exposure of medical personnel at work, sharing razors and toothbrushes, etc. can also be transmitted. Other infections, such as foot massage, tattooing, earring piercing, accidental exposure of medical personnel, sharing of razors and toothbrushes, can also be transmitted (III). Mother-to-child transmission mainly occurs during the perinatal (labor) period, mostly from contact with the blood and body fluids of HBV-positive mothers during delivery (Ⅰ), but with the use of hepatitis B vaccine combined with hepatitis B immunoglobulin, mother-to-child transmission has been greatly reduced. The risk of HBV infection increases with unprotected sexual contact with HBV-positive persons, especially those with multiple sexual partners (I). HBV is not transmitted through the respiratory and digestive tracts, so daily study, work or living contacts, such as working in the same office (including sharing office supplies such as computers), shaking hands, hugging, living in the same dormitory, eating in the same restaurant and sharing toilets without blood exposure, generally will not transmit HBV. epidemiological and experimental studies have not found that HBV can be transmitted through blood-sucking insects (mosquitoes, bedbugs, etc.). Third, the natural history. Age at the time of infection is the most important factor affecting chronicity. Among those infected with HBV during the perinatal (birth) period and infancy, 90% and 25%-30%, respectively, will develop chronic infection, while only 5-10% of those infected after the age of 5 will develop chronic infection (I). The natural history of HBV infection in infancy can generally be artificially divided into four phases, namely, the immune tolerance phase, the immune clearance phase, the inactive or low (non)-replication phase, and the reactivation phase. Immunotolerant phase: characterized by positive serum HBsAg and HBeAg, high HBV DNA load (often > 106 IU/mL, equivalent to 107 copies/mL), but normal serum alanine aminotransferase (ALT) levels, no significant abnormalities in liver histology that can be maintained for years or even decades, or mild inflammatory necrosis, no or only slow progression of liver fibrosis. Immunoclearance stage: manifested by serum HBV DNA titers > 2000 IU/mL (equivalent to 104 copies/mL), with persistent or intermittent elevation of ALT, moderate or severe inflammatory necrosis of liver histology, liver fibrosis can progress rapidly, and some patients can develop cirrhosis and liver failure. Inactive or low (non) replication stage: manifested by HBeAg negative, anti-HBe positive, HBV DNA consistently below 2000 IU/mL (equivalent to 104 copies/mL) or undetectable (PCR method), normal ALT levels, and no or only mild inflammation of liver histology; this is the result of immune control of HBV infection, and most patients in this stage have cirrhosis and The risk of HCC is greatly reduced, and in some patients who have sustained HBV DNA conversion for several years, the spontaneous HBsAg serological conversion rate is 1 to 3%/year. Reactive phase: Some patients in the inactive phase may have one or more episodes of hepatitis, mostly presenting as HBeAg negative, anti-HBe positive (partly due to low or no HBeAg expression levels caused by pre-C region and/or BCP variants), but still have active HBV DNA replication, persistent or recurrent abnormal ALT and become HBeAg negative chronic hepatitis B. These patients may progress to liver fibrosis, cirrhosis, decompensated cirrhosis and HCC; some patients may also develop spontaneous HBsAg disappearance (with or without anti-HBs) and reduced or undetectable HBV DNA, thus the prognosis is often good. A small number of patients at this stage can return to HBeAg-positive status (especially in immunosuppressed states such as when receiving chemotherapy). Not all people infected with HBV go through these four stages. Only a minority (about 5%) of HBV infections in the neonatal period result in spontaneous clearance of HBV, while most have a long period of immune resistance and then enter the immune clearance phase. However, most HBV infections in adolescence and adulthood do not have an immune tolerance period but enter directly into the immune clearance phase, and most of them can clear HBV spontaneously (about 90%-95%), while a minority (about 5%-10%) develop HBeAg-positive chronic hepatitis B. Spontaneous HBeAg serological conversion mainly occurs during the immune clearance period, with an annual incidence of about 2%-15%, with a higher incidence in those younger than 40 years old, with elevated ALT, and infected with HBV genotypes A and B. HBsAg clearance occurs in about 0.5%-1.0% per year after HBeAg serological conversion. The incidence of cirrhosis in patients with chronic HBV infection is related to the infection status. Patients in the immune tolerance phase have only very mild or no progression of liver fibrosis, whereas the immune clearance phase is a period of high incidence of cirrhosis. The cumulative incidence of cirrhosis is positively correlated with persistently high viral load, and HBV DNA is a risk factor independent of HBeAg and ALT that can independently predict the development of cirrhosis. Risk factors for the development of cirrhosis also include alcoholism, co-infection with HCV, HDV or HIV (I). Non-cirrhotic patients are less likely to develop primary hepatocellular liver cancer (HCC). HBeAg positivity and/or HBV DNA > 2,000 IU/mL (equivalent to 104 copies/mL) are significant risk factors for the development of cirrhosis and HCC in patients with cirrhosis. Large sample studies have shown that older age, male sex, and high ALT levels are also risk factors for the development of cirrhosis and HCC. family history of HCC is also a relevant factor, but HBV viral load is more important in the same genetic background.