Research progress on the role of endoplasmic reticulum stress in pathogenesis of hepatitis C virus infection

doi:10.16352/j.issn.1001-6325.2022.02.013

Abstract

Abstract: The infection caused by hepatitis C virus(HCV) often disturbs the momeostasis of endoplasmic reticulum. Accumulation of replication intermediates can lead to endoplasmic reticulum stress(ERS), which is closely related to the occurrence of many diseases. In order to prevent the harmful effects of endoplasmic reticulum stress, cells activate unfolded protein response(UPR) and apoptosis pathway. In early stage of virus infection, unfolded protein reaction is a main function to remove the proteins and other intermediates produced by the virus and when the infection deepens and the homeostasis is no longer to be maintained, the cell activates the apoptosis pathway. However, these pathways can also be manipulated by viral proteins to deepen infection and inhitit antiviral mechanism.

Key words: endoplasmic reticulum stress, unfolded protein response, hepatitis C virus, apoptosis

CLC Number:

R512.6⁺3

LI Ming-hao, FAN Liang-liang, XIANG Rong. Research progress on the role of endoplasmic reticulum stress in pathogenesis of hepatitis C virus infection[J]. Basic & Clinical Medicine, 2022, 42(2): 316-320.

References

[1]Alzahrani N, Wu MJ, Shanmugam S, et al. Delayed by design: role of suboptimal signal peptidase processing of viral structural protein precursors in flaviviridae virus assembly[J]. Viruses, 2020,12:1090. doi: 10.3390/v12101090.
[2]Ríos-Ocampo WA, Navas MC, Buist-Homan M, et al. Hepatitis C virus proteins core and NS5A are highly sensitive to oxidative stress-induced degradation after eIF2α/ATF4 pathway activation[J]. Viruses, 2020,12:425.doi:10.3390/v12040425.
[3]D'souza S, Lau KC, Coffin CS, et al. Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma[J]. World J Gastroenterol, 2020,26:5759-5783.
[4]Cansiz-Erson C, Kayisli UA, Guzel E. The role of unfolded protein response in the pathogenesis of endometriosis:contribution of peritoneal fluid[J]. Reprod Biomed Online, 2021,42:1-15.
[5]Aydin Y, Kurt R, Song K, et al. Hepatic stress response in HCV infection promotes STAT3-mediated inhibition of HNF4A-miR-122 feedback loop in liver fibrosis and cancer progression[J]. Cancers (Basel), 2019,11:1407. doi: 10.3390/cancers11101407.
[6]Huang W, Liao CC, Han Y, et al. Co-activation of Akt, Nrf2, and NF-κB signals under UPRER in torpid Myotis ricketti bats for survival[J]. Commun Biol, 2020,3:658. doi: 10.1038/s42003-020-01378-2.
[7]Hernandez C, Blanc EB, Pène V, et al. Impact of hepatitis C virus and alcohol, alone and combined, on the unfolded protein response in primary human hepatocytes[J]. Biochimie, 2020,168:17-27.
[8]Bashir S, Banday M, Qadri O, et al. The molecular mechanism and functional diversity of UPR signaling sensor IRE1[J]. Life Sci, 2020,11:118740.doi:10.1016/j.lfs.2020.118740.
[9]Zhao D, Yang J, Han K, et al. The unfolded protein response induced by Tembusu virus infection[J]. BMC Vet Res, 2019,15:34. doi: 10.1186/s12917-019-1781-4.
[10]Bao Y, Pu Y, Yu X,et al. IRE1B degrades RNAs encoding proteins that interfere with the induction of autophagy by ER stress in Arabidopsis thaliana[J]. Autophagy, 2018,14:1562-1573.
[11]Li S, Ye L, Yu X, et al. Hepatitis C virus NS4B induces unfolded protein response and endoplasmic reticulum overload response-dependent NF-kappaB activation[J]. Virology, 2009,391:257-264.
[12]Zheng Y, Gao B, Ye L, et al. Hepatitis C virus non-structural protein NS4B can modulate an unfolded protein response[J]. J Microbiol, 2005,43:529-536.
[13]Takahashi S, Sato N, Kikuchi J, et al. Immature core protein of hepatitis C virus induces an unfolded protein response through inhibition of ERAD-L in a yeast model system[J]. Genes Cells, 2017,22:160-173.
[14]Chan SW, Egan PA. Hepatitis C virus envelope proteins regulate CHOP via induction of the unfolded protein response[J]. FASEB J, 2005,19:1510-1512.
[15]Egan PA, Sobkowiak M, Chan SW. Hepatitis C virus envelope protein E1 binds PERK and represses the unfolded protein response[J]. Open Virol J, 2013,7:37-40.
[16]Yi S, Chen K, Zhang L,et al. Endoplasmic reticulum stress is involved in stress-induced hypothalamic neuronal injury in rats via the PERK-ATF4-CHOP and IRE1-ASK1-JNK pathways[J]. Front Cell Neurosci, 2019,13:190. doi: 10.3389/fncel.2019.00190.
[17]Takaki H, Akazawa Y, Kido Y,et al. Hepatitis C virus infection increases c-Jun N-terminal kinase (JNK) phosphorylation and accentuates hepatocyte lipoapoptosis[J]. Med Sci Monit, 2017,23:4526-4532.
[18]Ma X, Yu M, Hao C, et al. Shikonin induces tumor apoptosis in glioma cells via endoplasmic reticulum stress, and Bax/Bak mediated mitochondrial outer membrane permeability[J]. J Ethnopharmacol, 2020,263:113059. doi: 10.1016/j.jep.2020.113059.
[19]Poole MI, Sorribes I, Jain HV. Modeling hepatitis C virus protein and p53 interactions in hepatocytes: Implications for carcinogenesis[J]. Math Biosci, 2018,306:186-196.
[20]Yao Z, Song X, Cao S, et al. Role of the exogenous HCV core protein in the interaction of human hepatocyte proliferation and macrophage sub-populations[J]. PLoS One, 2014,9:e108278. doi: 10.1371/journal.pone.0108278.
[21]Axley P, Ahmed Z, Ravi S, et al. Hepatitis C virus and hepatocellular carcinoma: a narrative review[J]. J Clin Transl Hepatol, 2018,6:79-84.
[22]Boyer A, Dreneau J, Dumans A, et al. Endoplasmic reticulum detergent-resistant membranes accommodate hepatitis C virus proteins for viral assembly[J]. Cells, 2019,8:487. doi: 10.3390/cells8050487.
[23]Ríos-Ocampo WA, Daemen T, Buist-Homan M, et al. Hepatitis C virus core or NS3/4A protein expression preconditions hepatocytes against oxidative stress and endoplasmic reticulum stress[J]. Redox Rep, 2019,24:17-26.
[24]Javed F, Manzoor S. HCV non-structural NS4A protein of genotype 3a induces mitochondria mediated death by activating Bax and the caspase cascade[J]. Microb Pathog, 2018,124:346-355.
[25]Xie Z, Xiao Z, Wang F. Hepatitis C virus nonstructural 5A protein (HCV-NS5A) inhibits hepatocyte apoptosis through the NF-κb/miR-503/bcl-2 pathway[J]. Mol Cells, 2017,40:202-210.
[26]Quan M, Liu S, Zhou L,et al. Hepatitis C virus nonstructural 5A protein inhibits the starvation induced apoptosis of hepatoblastoma cells by increasing Beclin 1 expression[J]. Oncol Rep, 2019,41:3051-3059.
[27]Li S, Kong L, Yu X. The expanding roles of endoplasmic reticulum stress in virus replication and pathogenesis[J]. Crit Rev Microbiol, 2015,41:150-164.