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CN 34-1304/RISSN 1674-3679

Volume 29 Issue 2
Feb.  2025
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CHEN Yifan, CAO Guangwen. Molecular epidemiological characteristics and specific prophylactic and control strategy of hepatitis B[J]. CHINESE JOURNAL OF DISEASE CONTROL & PREVENTION, 2025, 29(2): 125-131. doi: 10.16462/j.cnki.zhjbkz.2025.02.001
Citation: CHEN Yifan, CAO Guangwen. Molecular epidemiological characteristics and specific prophylactic and control strategy of hepatitis B[J]. CHINESE JOURNAL OF DISEASE CONTROL & PREVENTION, 2025, 29(2): 125-131. doi: 10.16462/j.cnki.zhjbkz.2025.02.001

Molecular epidemiological characteristics and specific prophylactic and control strategy of hepatitis B

doi: 10.16462/j.cnki.zhjbkz.2025.02.001
Funds:

National Natural Science Foundation of China 82473715

Three-Year Public Health Program of the Shanghai Health Commission GWV-10.1-XK17

More Information
  • Corresponding author: CAO Guangwen, E-mail: gcao@smmu.edu.cn
  • Received Date: 2024-11-11
  • Rev Recd Date: 2025-01-07
  • Available Online: 2025-03-08
  • Publish Date: 2025-02-10
  • Currently, there are approximately 257 million individuals globally infected with hepatitis B virus (HBV). In mainland China, about 75 million residents are chronically infected with HBV. Furthermore, the infection rate of HBV is 7.54% among those aged over 30 years. The prevalence of HBV infection is higher in rural areas than in urban areas. The highest rate of HBV infection is evident in the central and southern China. HBV has 10 genotypes, among which genotype B and C are endemic in China. Genotype B HBV is more apt to transmit horizontally in the young and cause acute hepatitis B, whereas genotype C HBV is more apt to cause intrafamilial transmission and induce liver cirrhosis and hepatocellular carcinoma (HCC). HBV vaccination effectively prevents the occurrences of chronic HBV infection, liver cirrhosis, and HCC. Chronic HBV infection accounts for 84.4% of HCC causes in mainland China. HBV promotes hepatocarcinogenesis via high replication, mutation and viral integration into the host genome. High replication of HBV activates and maintains inflammatory microenvironment that induces and selects the hepatocytes with somatic mutations and mutated HBV. Compared to the wild type, the oncogenic potential of HBV is significantly enhanced in mutated forms. The mutated HBV promotes the retro-differentiation of the mutated hepatocytes via activating key signaling pathways in the inflammatory microenvironment. HBV integration facilitates the selective growth advantage of the mutated hepatocytes via inactivating tumor suppressors and activating human telomerase reverse transcriptase. The high-risk HBV mutations can predict the occurrence, postoperative prognosis, and prophylactic effect of antiviral treatments. Antiviral treatments are able to significantly decrease the occurrence and postoperative prognosis, especially in those carrying HBV mutations in the core promoter region, thus fulfilling the specific prophylaxis and control of HBV-related HCC.
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