Abstract
The ended COVID-19 pandemic has resulted in the infection and death of millions of people. According to the WHO, the coronavirus pandemic lasted 3 years, 1 month, and 24 days and claimed the lives of 6.9 million people. The disease is mainly spread through airborne droplets and aerosols. Coronaviruses have the largest genomes among all RNA viruses that encode structural and nonstructural proteins, ensuring their persistence in various environmental niches and hosts. Evolving viral proteins facilitate host recognition and penetration, genome replication, assembly and release of progeny viruses, and evasion of host immune surveillance. In addition, SARS-CоV-2 can inhibit the host's innate antiviral response, thereby triggering hyperinflammatory reactions, resulting in severe COVID-19 infection. Increased expression of inhibitory receptors by SARS-CоV-2 leads to exhaustion and loss of host effector T cell functions. Meanwhile, long-term immunosuppression provokes persistent inflammation, immunosuppression, and catabolism syndrome and long COVID or post COVID. SARS-CoV-2 infection has a powerfully destructive impact on the economy and healthcare, resulting in an unprecedented scientific response. In this paper, we provide a framework for understanding multistep SARS-CoV-2 penetration that facilitates its efficient transmission to humans. KEYWORDS: coronaviruses, COVID-19, SARS-CoV-2, pandemic, long COVID, post COVID. FOR CITATION: Pechkurov D.V., Romanova A.A., Savvateeva O.A., Tyazheva A.A., Gorelov A.V. SARS-CоV-2: what allowed the virus to cause a long-term pandemic? Russian Medical Inquiry. 2023;7(11):742–750 (in Russ.). DOI: 10.32364/2587-6821-2023-7-11-7.
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