Department of Microbiology, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran.
Antimicrobial Resistance Research Center, Bu Ali Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, IR Iran.
Virus Res. 2018 Feb 2;245:29-43. doi: 10.1016/j.virusres.2017.12.007. Epub 2017 Dec 19.
Hepatitis B virus (HBV) infection is a leading cause of liver damage and hepatic inflammation. Upon infection, effective antiviral responses by CD8+ T cells, CD4+ T cells, Natural killer (NK) cells, and monocytes can lead to partial or complete eradication of the viral infection. To date, many studies have shown that the production of inhibitory cytokines such as Interleukin 10 (IL-10), Transforming growth factor beta (TGF-β), along with dysfunction of the dendritic cells (DCs), and the absence of efficient innate immune responses could lead to T cell exhaustion, development of persistent infection, and inability to eradicate the viral infection from liver. Understanding the immunopathogenesis of the virus could be useful in providing further insights toward novel strategies in the eradication of HBV infection.
乙型肝炎病毒(HBV)感染是导致肝损伤和肝炎症的主要原因。在感染后,CD8+ T 细胞、CD4+ T 细胞、自然杀伤(NK)细胞和单核细胞的有效抗病毒反应可导致部分或完全清除病毒感染。迄今为止,许多研究表明,抑制性细胞因子(如白细胞介素 10(IL-10)、转化生长因子β(TGF-β)的产生以及树突状细胞(DCs)功能障碍和有效的先天免疫反应缺失可能导致 T 细胞耗竭、持续性感染的发展以及无法从肝脏中清除病毒感染。了解病毒的免疫发病机制可能有助于为根除 HBV 感染提供新的策略。