ABSTRACT
Coronavirus disease 19 (COVID-19), is a complex and heterogeneous medical entity. It is caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). SARS-CoV-2 is an RNA virus similar to the SARS-CoV-1 and MERS-CoV viruses. COVID-19 disease is predominantly respiratory, but it can involve multiple systems. Although it may be asymptomatic or produce few symptoms in most infected patients, 20 % of those affected have severe or fatal disease with respiratory or/and multiple organ failure. The elimination of SARS-CoV-2 requires innate and adaptive immune responses, highlighting the importance of interferons, Toll-like receptors, serum complement, the response of T lymphocytes, and the formation of neutralizing antibodies against the virus. In a significant proportion of patients with severe COVID-19, the presence of primary immunodeficiencies (especially in the interferon pathway and T-lymphocyte signaling) has been described. Autoantibodies against various immunomodulatory proteins (cytokines, especially anti-interferons, chemokines, complement, and cell surface proteins), and antinuclear and antiphospholipid antibodies have also been reported. Autoimmune diseases can appear in the convalescent phase. Immunodeficiency and autoimmunity are responsible for viral escape and prolonged COVID. © 2022 Academia Nacional de Medicina. All rights reserved.
ABSTRACT
At the end of 2019, a new pathogen, coronavirus SARS-CoV2, was identified. The virus has infected more than 30 million people worldwide with lethality close to 5 %. SARS-CoV2 is an RNA virus. The viral genome contains 29 891 nucleotides which encode 9 889 amino acids;5´-replicase (orf1/ab) four main structural proteins [Spike (S) -Envelope (E) - Membrane (M) -Nucleocapsid (N)] and open reading frame proteins. MicroRNAs (miRNA) are potent post-transcriptional regulators of gene expression and hence can control viral infection and replication. In silico and bioinformatics assessments revealed that host miRNA (15b-5p, 15a-5p, 197-5p, 548c-5p, 548d-5p, 409-3p, 30b-5p, 505-3p) may be involved blocking viral replication. Also, viral miRNA are shared with cells miRNA (8066, 5197, 3611, 3934-3p, 1307-3p, 3691-3p, 1468-5p), which may modulate cell response and facilitate SARS-CoV2 infection. Even though, these targets have to be validated with studies in vitro and in vivo, there is a high therapeutic potential involved which has been proposed and tested in other viral infections. More studies on the molecular mechanism of this complex viral infection are required to understand viral pathogenesis. © 2020 Academia Nacional de Medicina. All rights reserved.