Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors
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REVIEW
Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors A. V. Zamaraev1, B. Zhivotovsky1,2, and G. S. Kopeina1,a* 1 2
Faculty of Basic Medicine, Lomonosov Moscow State University, 119192 Moscow, Russia Institute of Environmental Medicine, Karolinska Institute, SE171 77 Stockholm, Sweden a email: [email protected] Received June 30, 2020 Revised September 9, 2020 Accepted September 9, 2020
Abstract—The disruption of apoptotic cell death process is closely associated with the etiology of various diseases, includ ing cancer. Permanent viral infections can cause different types of cancers. Oncogenic viruses manipulate both external and internal apoptosis pathways, and inhibit the activity of proapoptotic proteins and signaling pathways, which facilitates car cinogenesis. Ineffective immune surveillance or immune response suppression can induce uncontrolled virus propagation and host cell proliferation. In this review, we discuss current data that provide insights into mechanisms of apoptotic death suppression by viruses and their role in oncogenesis. DOI: 10.1134/S0006297920100077 Keywords: oncogenic viruses, apoptosis, carcinogenesis
INTRODUCTION In multicellular organisms apoptosis plays an impor tant role in the maintenance of cellular homeostasis, morphogenesis, and is also involved in various stages of development, immune system functioning, and the removal of damaged or infected cells [1]. The initiation of apoptosis is triggered by extracellular or intracellular fac tors, such as activation of death receptors, disturbance in the cell cycle signals, accumulation of misfolded proteins, DNA damage, metabolic disorders, and various bacterial and viral infections. There are two main apoptosis signaling pathways: the extrinsic (receptordependent signaling pathway involv Abbreviations: AIF, apoptosis inducing factor; Akt, protein kinase B; CD95/Fas/Apo1, death receptor; cIAP, cellular inhibitor of apoptosis proteins; DISC, death inducing signaling complex; EBV, Epstein–Barr virus; FADD, Fasassociated protein with death domain; HBx, hepatitis B virus protein; HIV1, Human Immunodeficiency Virus; HPV, human papillomavirus; HTLV 1, retrovirus of human Tcell leukemia type 1; KSHV, herpesvirus associated with Kaposi’s sarcoma; NFκB, nuclear transcription factor kappaB; PI3K, phosphatidylinositol 3kinase; SARS CoV, positivesense singlestranded RNA virus of the coronavirus family; TNF, tumor necrosis factor; TNFR1, tumor necrosis fac tor receptor 1; TRADD, TNFR1associated death domain pro tein; ROS, reactive oxygen species. * To whom correspondence should be addressed.
ing death receptors) and the intrinsic (mitochondrial) pathway. The extrinsic pathway is initiated by interactions between specific death ligands and death receptors [CD95, TRAILR1/2, and tumor necrosis factor receptor 1 (TNFR1)] on the cell surface. Ligands interacting with the receptors promote receptor oligomerization and con formational changes that facilitate binding to the adaptor proteins [Fasassociate
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