I. Pathogenesis Hepatitis B virus (HBV) belongs to the family of hepatophilic DNA viruses (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°C for 10 h, boiling for 10 min or high-pressure steam. effect. After HBV invades hepatocytes, part of the double-stranded cyclic HBV DNA is used in the nucleus as a template to extend the positive strand to repair the gap area in the positive strand, 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 be completely removed from the body [2, 3]. HBV has been found to have nine genotypes from A to I [4, 5], with types C and B predominating in China. HBV genotype is associated with disease progression and the effect of interferon alpha therapy. Compared with those infected with genotype C, those infected with genotype B showed earlier HBeAg serological conversion and less progression to chronic hepatitis, cirrhosis and primary hepatocellular carcinoma [6-9]; and the response rate to interferon α therapy was higher in HBeAg-positive patients than in genotype C; patients with genotype A were higher than those with genotype D [10-12]. II. 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, of which 350 million are chronically infected with HBV, and about 1 million people die each year from liver failure, cirrhosis and primary hepatocellular carcinoma (HCC) caused by HBV infection [13, 14]. The 2006 national epidemiological survey of hepatitis B showed that the HBsAg carriage rate in the general population aged 1-59 years in China was 7.18% and only 0.96% in children under 5 years old [15, 16]. According to this projection, the existing chronic HBV infection in China is about 93 million people, including about 20 million cases of chronic hepatitis B [17]. 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 strict HBsAg screening of 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 injection; other infections such as pedicure, tattoo, earring piercing, accidental exposure of medical personnel at work, sharing razors and toothbrushes, etc. can also be transmitted (III). (III) can also be transmitted. Mother-to-child transmission occurs mainly during the perinatal period, mostly from exposure to 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 [18]. Unprotected sexual contact with HBV-positive persons, especially those with multiple partners, increases the risk of HBV infection (I). HBV is not transmitted through the respiratory and gastrointestinal 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 do not transmit HBV. The epidemiological and experimental studies have also not found that HBV can be transmitted by blood-sucking insects (mosquitoes, bedbugs, etc.)[19] . 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 5 years of age will develop chronic infection [20] (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 [[21]. 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, and liver histology without significant abnormalities that can be maintained for years or even decades [22], or mild inflammatory necrosis with no or only slow progression of liver fibrosis. Immunoclearance phase: 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 may progress rapidly, and some patients may 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 a much reduced risk of 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 experience one or several episodes of hepatitis, mostly presenting as HBeAg negative and 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 and persistent or recurrent abnormal ALT, becoming HBeAg negative chronic hepatitis B [ 23], and these patients can progress to liver fibrosis, cirrhosis, decompensated cirrhosis and HCC; some patients can also develop F spontaneous HBsAg disappearance (with or without anti-HBs) and reduced or undetectable HBV DNA, and thus the prognosis is often good. A small number of patients in 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 immune resistance period followed by an immune clearance period. However, most adolescents and adults infected with HBV during adolescence do not have an immune tolerance period but enter directly into the immune clearance phase, and most of them can spontaneously clear HBV (about 90%-95%), while a few (about 5%-10%) develop HBeAg-positive chronic hepatitis B. Spontaneous HBeAg serologic conversion occurs mainly during the immune clearance phase, with an annual incidence of approximately 2%-15%, with a higher incidence in those younger than 40 years of age, with elevated ALT, and infected with HBV genotypes A and B [21, 24]. HBsAg clearance occurs in approximately 0.5%-1.0% per year after HBeAg serologic conversion [25]. 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 [26-28] (I). Non-cirrhotic patients are less likely to develop primary hepatocellular liver cancer (HCC). Its annual incidence in patients with cirrhosis is 3-6% [29-31]. 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 [8, 32-35]. Studies with large samples have shown that older age, male gender, and high ALT levels are also risk factors for the development of cirrhosis and HCC [25, 33]. family history of HCC is also a relevant factor, but HBV viral load is more important in the same genetic background [36] (II-3). IV. Prevention (i) Hepatitis B vaccine prevention Vaccination against hepatitis B is the most effective way to prevent HBV infection. The targets of hepatitis B vaccination are mainly newborns [37], followed by infants and children, unimmunized people under 15 years of age and high-risk groups (e.g., medical personnel, people with frequent exposure to blood, workers in childcare institutions, organ transplant patients, frequent recipients of blood transfusions or blood products, immunocompromised people, people prone to trauma, family members of HBsAg-positive people, men who have sex with men or multiple sexual partners, and people who inject drugs intravenously). The vaccine should be administered to all patients (including those who have multiple sexual partners and those who inject drugs intravenously, etc.). Three doses of hepatitis B vaccine are required for the entire course, according to the 0, 1, and 6 months procedure, i.e., after the first dose of vaccine, the second and third doses of vaccine are given at intervals of 1 month and 6 months. Hepatitis B vaccination for newborns should be given within 24 hours of birth, the earlier the better. The site of vaccination is intramuscular in the lateral anterior gluteal muscle for newborns and intramuscular in the middle deltoid muscle of the upper arm for children and adults. The blockage rate of mother-to-child transmission with hepatitis B vaccine alone was 87.8% [38] (II-3). Newborns of HBsAg-positive mothers should be given hepatitis B immunoglobulin (HBIG) at a dose of ≥100 IU as early as possible within 24 h after birth (preferably 12 h after birth), along with 10 μg recombinant yeast or 20 μg Chinese hamster oocyte (CHO) hepatitis B vaccine at different sites, and a second and third dose of hepatitis B vaccine at 1 and 6 months of age, respectively. The effectiveness of interruption of mother-to-child transmission is significantly improved with hepatitis B vaccination at 1 and 6 months of age [37, 38] (II-3). It is also possible to administer one dose of HBIG within 12 h of birth, followed by a second dose of HBIG 1 month later, and one 10 μg recombinant yeast or 20 μg CHO hepatitis B vaccine at different sites at the same time, with the second and third doses of hepatitis B vaccine at 1 and 6 months intervals, respectively [39]. Newborns can receive breastfeeding from HBsAg-positive mothers after HBIG and hepatitis B vaccine administration within 12 h of birth [40, 41] (III). Newborns of HBsAg-negative mothers can be immunized with 5 μg or 10 μg yeast or 10 μg CHO hepatitis B vaccine; children who were not vaccinated against hepatitis B during the neonatal period should receive a catch-up vaccination with 5 μg or 10 μg recombinant yeast or 10 μg CHO hepatitis B vaccine; for adults, 20 μg yeast or 20 μg CHO hepatitis B vaccine is recommended. For those who are immunocompromised or non-responders, the vaccination dose (e.g. 60 μg) and number of doses should be increased; for those who do not respond to the 3-dose immunization program, they can receive 3 more doses and have their serum tested for anti-HBs 1~2 months after the second 3-dose hepatitis B vaccine, and if they still do not respond, they can receive one 60 μg recombinant yeast hepatitis B vaccine.