Autophagy is involved in the pathogenesis of multiple pathogen infection. Previous studies have reported that human cytomegalovirus (CMV) activates autophagy in the early stage of infection and then inhibits autophagy. Little is known about the role of autophagy in murine CMV (MCMV) infection, especially in MCMV-induced hepatitis. The purpose of this study is to investigate the role of autophagy in MCMV hepatitis. BALB/c mice were infected with MCMV and a series of experiments involving western blot, immunofluorescence, immunohistochemistry, H&E (Hematoxylin and Eosin) staining and quantitative real-time polymerase chain reaction were performed in this study. The expression of SQSTM1/p62, PI3K, the ratio of phosphorylated Akt to total Akt, and the ratio of phosphorylated mammalian target of rapamycin (mTOR) to total mTOR were increased, and the expression of light-chain 3 (LC3)-II were decreased in the livers of infected mice on days 3 and 7 postinfection (p.i.). Compared with the untreated infected group, increased transcription level of MCMV glycoprotein B (gB), increased expression levels of interleukin1-β (IL-1β), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), decreased expression level of type I interferon α (IFN-α), as well as aggravated liver pathological injury were detected in starvation-treated infected group on days 3 and 7 p.i.; whereas decreased transcription level of MCMV gB, decreased expression levels of IL-1β, AST and ALT, increased expression level of type I IFN-α, as well as alleviated liver pathological injury were detected in chloroquine (CQ)-treated infected group on day 3 p.i. In conclusion, autophagy is inhibited through activating the PI3K/Akt/mTOR pathway in the liver of BALB/c mice during MCMV infection, and autophagy may promote MCMV replication and aggravate liver pathological damage and inflammation. Further understanding of the interactions between autophagy and MCMV infection and its potential mechanism may bring new important cues to the control of MCMV infection and antiviral therapy.

中文翻译：

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自噬在小鼠巨细胞病毒肝炎中的作用

自噬参与多种病原体感染的发病机制。以往的研究报道，人类巨细胞病毒（CMV）在感染早期激活自噬，然后抑制自噬。关于自噬在小鼠CMV中的作用知之甚少(MCMV) 感染，尤其是在 MCMV 引起的肝炎中。本研究的目的是探讨自噬在 MCMV 肝炎中的作用。本研究采用 MCMV 感染 BALB/c 小鼠，并进行了一系列实验，包括蛋白质印迹、免疫荧光、免疫组织化学、H&E（苏木精和曙红）染色和定量实时聚合酶链反应。SQSTM1/p62、PI3K、磷酸化 Akt 与总 Akt 比值、磷酸化哺乳动物雷帕霉素靶蛋白 (mTOR) 与总 mTOR 比值升高，轻链 3 (LC3)-II 表达升高。在感染后第 3 天和第 7 天 (pi)，受感染小鼠的肝脏中减少。与未治疗的感染组相比，MCMV 糖蛋白 B (gB) 的转录水平增加，饥饿时检测到白细胞介素1-β（IL-1β）、天冬氨酸氨基转移酶（AST）和丙氨酸氨基转移酶（ALT）表达水平升高，I型干扰素α（IFN-α）表达水平降低，肝脏病理损伤加重-在感染后第 3 天和第 7 天接受治疗的感染组；而氯喹（CQ）治疗感染组当天检测到MCMV gB转录水平降低，IL-1β、AST和ALT表达水平降低，I型IFN-α表达水平升高，肝脏病理损伤减轻3 pi 总之，MCMV感染期间BALB/c小鼠肝脏通过激活PI3K/Akt/mTOR通路抑制自噬，自噬可能促进MCMV复制，加重肝脏病理损伤和炎症。