乙肝病毒e抗原與病毒存留☆

StephenW

乙肝病毒e抗原與病毒存留☆
Kuen-NanTsai, Jing-Hsiung James Ou

    南加州大學凱克醫學院分子微生物學和免疫學系，2011 Zonal Avenue, HMR-401, Los Angeles, CA, 90033, USA

2021 年 10 月 28 日在線提供。
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https://doi.org/10.1016/j.coviro.2021.10.003
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強調

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    母體 HBeAg 影響後代的庫普弗細胞以促進 HBV 的持續存在。
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    HBeAg 與調節性 T 細胞相互作用以抑制自然殺傷細胞的活性。
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    HBeAg 抑制死亡受體介導的細胞凋亡。
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    HBeAg 干擾 TLR 2、NF-κB 和 I 型乾擾素的先天免疫信號。

近50年前，乙型肝炎病毒（HBV）e抗原（HBeAg）在HBV患者的血清中被發現。 HBV 在肝細胞中感染或複制不是必需的。早期的臨床研究表明，這種抗原可能對 HBV 在母嬰傳播後在嬰兒中的持續存在發揮重要作用。隨後的臨床研究還表明 HBeAg 可能具有免疫調節活性。近年來，發表了大量關於 HBeAg 如何調節宿主免疫的信息。在這篇綜述中，我們總結了 HBeAg 免疫調節活性的最新研究進展，並討論了 HBeAg 的這些活性如何促進 HBV 的持續存在。

StephenW

Hepatitis B virus e antigen and viral persistence☆
Kuen-NanTsai, Jing-Hsiung James Ou

    Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, 2011 Zonal Avenue, HMR-401, Los Angeles, CA, 90033, USA

Available online 28 October 2021.
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https://doi.org/10.1016/j.coviro.2021.10.003
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Highlights

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    Maternal HBeAg impacts Kupffer cells of the offspring to promote HBV persistence.
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    HBeAg interacts with regulatory T cells to suppress natural killer cell activity.
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    HBeAg suppresses death receptor-mediated apoptosis.
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    HBeAg perturbs innate immune signaling of TLR 2, NF-κB and type I interferons.

Hepatitis B virus (HBV) e antigen (HBeAg) was discovered in the sera of HBV patients nearly 50 years ago. It is not essential for HBV to infect or replicate in hepatocytes. Earlier clinical studies suggested that this antigen might play an important role for HBV to establish persistence in babies after its mother-to-child transmission. Subsequent clinical studies also suggested that HBeAg might have immunomodulatory activities. In recent years, a large body of information on how HBeAg might modulate host immunity was published. In this review, we summarize recent research progresses on the immunomodulatory activities of HBeAg and discuss how these activities of HBeAg may promote HBV persistence.