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Immunoediting in Sars-Cov-2: Mutual Relationship Between the Virus and the Host Publisher Pubmed



Kheshtchin N1, 2 ; Bakhshi P3 ; Arab S4, 5 ; Nourizadeh M6
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  2. 2. Allergy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
  3. 3. Department of Medical Biotechnology, Faculty of Allied Medical Sciences, Iran University of Medical Sciences, Tehran, Iran
  4. 4. Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran
  5. 5. Department of Tissue Engineering and Applied Cell Sciences, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran
  6. 6. Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran

Source: International Immunopharmacology Published:2022


Abstract

Immunoediting is a well-known concept that occurs in cancer through three steps of elimination, equilibrium, and escape (3Es), where the immune system first suppresses the growth of tumor cells and then promotes them towards the malignancy. This phenomenon has been conceptualized in some chronic viral infections such as HTLV-1 and HIV by obtaining the resistance to elimination and making a persistent form of infected cells especially in untreated patients. Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a heterogeneous disease characterizing from mild/asymptomatic to severe/critical courses with some behavioral aspects in an immunoediting setting. In this context, a coordinated effort between innate and adaptive immune system leads to detection and destruction of early infection followed by equilibrium between virus-specific responses and infected cells, which eventually ends up with an uncontrolled inflammatory response in severe/critical patients. Although the SARS-CoV-2 applies several escape strategies such as mutations in viral epitopes, modulating the interferon response and inhibiting the MHC I molecules similar to the cancer cells, the 3Es hallmark may not occur in all clinical conditions. Here, we discuss how the lesson learnt from cancer immunoediting and accurate understanding of these pathophysiological mechanisms helps to develop more effective therapeutic strategies for COVID-19. © 2022 Elsevier B.V.
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