乙型肝炎病毒激活 AIM2 可产生抗病毒免疫，从而在合并感染时抑制丙型肝炎病毒。
Activation of AIM2 by hepatitis B virus results in antiviral immunity that suppresses hepatitis C virus during coinfection.
机构信息
Institute of Translational Medicine, The First Hospital of Jilin University , Changchun, Jilin, China.
Hunan Provincial Key Laboratory of Medical Virology, State Key Laboratory of Chemo/Biosensing and Chemometrics, Institute of Pathogen Biology and Immunology of College of Biology, Hunan University , Changsha, Hunan, China.
出版信息
J Virol. 2023 Oct 31;97(10):e0109023. doi: 10.1128/jvi.01090-23. Epub 2023 Oct 3.
Clinical data suggest that Hepatitis C virus (HCV) levels are generally lower in Hepatitis B virus (HBV) co-infected patients, but the mechanism is unknown. Here, we show that HBV, but not HCV, activated absent in melanoma-2. This in turn results in inflammasome-mediated cleavage of pro-IL-18, leading to an innate immune activation cascade that results in increased interferon-γ, suppressing both viruses.
临床数据表明，乙型肝炎病毒 (HBV) 合并感染患者的丙型肝炎病毒 (HCV) 水平通常较低，但具体机制尚不清楚。在这里，我们发现乙型肝炎病毒（HBV）而非丙型肝炎病毒（HCV）能够激活黑素瘤缺失蛋白 2（AIM2）。这反过来导致炎性体介导致 pro-IL-18 的切割，引发先天免疫激活级联反应，导致干扰素-γ增加，从而抑制两种病毒。
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