生物
乙型肝炎病毒
免疫
病毒学
免疫学
HBeAg
传输(电信)
病毒
免疫系统
乙型肝炎
慢性感染
病毒复制
乙型肝炎表面抗原
电气工程
工程类
作者
Kuen Nan Tsai,Cheng-Fu Kuo,Jing-Hsiung Ou
标识
DOI:10.1016/j.tim.2017.07.006
摘要
HBV frequently causes chronic infection after vertical transmission but mostly self-limited acute infection after horizontal transmission. HBV harnesses type I interferon immune response to enhance its own replication. HBV persistence is affected by the age of infection, size of viral inoculum, and gut microbiota. Maternal HBeAg can train Kupffer cells of the offspring, likely in utero, to suppress HBV-specific CD8+ T cells in the presence of HBeAg after birth. Hepatitis B virus (HBV) chronically infects 250 million people worldwide, resulting in nearly one million deaths annually. Studies in recent years have significantly improved our knowledge on the mechanisms of HBV persistence. HBV uses multiple pathways to harness host innate immunity to enhance its replication. It can also take advantage of the developing immune system and the not-yet-stabilized gut microbiota of young children to facilitate its persistence, and use maternal viral e antigen to educate immunity of the offspring to support its persistence after vertical transmission. The knowledge gained from these recent studies paves the way for the development of new therapies for the treatment of chronic HBV infection, which has so far been very challenging. Hepatitis B virus (HBV) chronically infects 250 million people worldwide, resulting in nearly one million deaths annually. Studies in recent years have significantly improved our knowledge on the mechanisms of HBV persistence. HBV uses multiple pathways to harness host innate immunity to enhance its replication. It can also take advantage of the developing immune system and the not-yet-stabilized gut microbiota of young children to facilitate its persistence, and use maternal viral e antigen to educate immunity of the offspring to support its persistence after vertical transmission. The knowledge gained from these recent studies paves the way for the development of new therapies for the treatment of chronic HBV infection, which has so far been very challenging. community of microorganisms living in digestive tracts. serological change from HBeAg-positive to anti-HBeAg antibody-positive during chronic HBV infection. transmission of the virus between two individuals, usually between adults. injection of a high volume of saline via the tail vein of mice within a short duration of 5–8 s. resident macrophages of the liver. the progressive loss of T cell functions. transgenic mice with severe combined immunodeficiency and hepatocyte-specific expression of urokinase-type plasminogen activator. transmission of the virus from a mother to her children.
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