Hossein Khorramdelazad, Mohammad Hossein Kazemi, Maryam Azimi, Azin Aghamajidi, Ali Zarezadeh Mehrabadi, Faezeh Shahba, Nazanin Aghamohammadi, Reza Falak, Fatemeh Faraji, Reza Jafari
European journal of pharmacology 2022 Jul 15Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is currently the major global health problem. Still, it continues to infect people globally and up to the end of February 2022, over 436 million confirmed cases of COVID-19, including 5.95 million deaths, were reported to the world health organization (WHO). No specific treatment is currently available for COVID-19, and the discovery of effective therapeutics requires understanding the effective immunologic and immunopathologic mechanisms behind this infection. Type-I interferons (IFN-Is), as the critical elements of the immediate immune response against viral infections, can inhibit the replication and spread of the viruses. However, the available evidence shows that the antiviral IFN-I response is impaired in patients with the severe form of COVID-19. Moreover, the administration of exogenous IFN-I in different phases of the disease can lead to various outcomes. Therefore, understanding the role of IFN-I molecules in COVID-19 development and its severity can provide valuable information for better management of this disease. This review summarizes the role of IFN-Is in the pathogenesis of COIVD-19 and discusses the importance of autoantibodies against this cytokine in the spreading of SARS-CoV-2 and control of the subsequent excessive inflammation. Copyright © 2022 Elsevier B.V. All rights reserved.
Hossein Khorramdelazad, Mohammad Hossein Kazemi, Maryam Azimi, Azin Aghamajidi, Ali Zarezadeh Mehrabadi, Faezeh Shahba, Nazanin Aghamohammadi, Reza Falak, Fatemeh Faraji, Reza Jafari. Type-I interferons in the immunopathogenesis and treatment of Coronavirus disease 2019. European journal of pharmacology. 2022 Jul 15;927:175051
PMID: 35618037
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