MTOR Signaling: The Interface Linking Cellular Metabolism and Hepatitis B Virus Replication

Zhongji Meng,Mengji Lu,Xueyu Wang,Yongfang Jiang,Zhiqiang Wei

doi:10.1007/s12250-021-00450-3

Abstract

Mammalian target of rapamycin (mTOR) is a conserved Ser/Thr kinase that includes mTOR complex (mTORC) 1 and mTORC2. The mTOR pathway is activated in viral hepatitis, including hepatitis B virus (HBV) infection-induced hepatitis. Currently, chronic HBV infection remains one of the most serious public health issues worldwide. The unavailability of effective therapeutic strategies for HBV suggests that clarification of the pathogenesis of HBV infection is urgently required. Increasing evidence has shown that HBV infection can activate the mTOR pathway, indicating that HBV utilizes or hijacks the mTOR pathway to benefit its own replication. Therefore, the mTOR signaling pathway might be a crucial target for controlling HBV infection. Here, we summarize and discuss the latest findings from model biology research regarding the interaction between the mTOR signaling pathway and HBV replication.

Highlights

Hepatitis B virus (HBV) infection remains a global threat to public health
Our recent study demonstrated that HBV inhibited lysosomal activity is restored to enhance HBV antigens degradation by inhibiting Akt/Mammalian target of rapamycin (mTOR) signaling after silencing CCDC88A in hepatoma cells with HBV replication (Wang et al 2021)
We have summarized recent progress from studies on the interaction between the cellular mTOR signaling pathway and HBV replication. mTOR first attracted the attention of researchers because it may play important roles in the development of HBV-associated hepatocellular carcinoma (HCC)

Summary

Introduction

Hepatitis B virus (HBV) infection remains a global threat to public health. Patients with chronic HBV infection are prone to cirrhosis, liver failure, and hepatocellular carcinoma (HCC) (Tang et al 2018). HBV-Mediated Activation of mTOR Signaling Pathway mTOR signaling is a key regulator of many cellular processes including metabolism, proliferation and survival. HBV infection can induce the synthesis of a large quantity of viral proteins and lead to the accumulation of HBsAg in the ER lumen to trigger ER stress, thereby activating the PI3K/Akt/mTOR pathway (Choi et al 2019).

Results

Conclusion