A Review of the Mechanisms Involved in the Immunopathogenesis of SARS-CoV-2

Coronaviruses belong to the Coronaviridae family and three SARS-CoV, MERS-CoV and SARS-CoV-2 pathogens are found in this family, all of which cause respiratory disorders in human beings. SARS-CoV-2 is a RNA virus of approximately 80-160 nm in size and genomic size of approximately 27-35 kb which causes COVID-19. Symptoms of COVID-19 include fever, dry cough, fatigue and muscle weakness, shortness of breath, sputum, headache, diarrhea and muscle inflammation. It causes death in the elderly, people with hypertension, a history of cardiovascular diseases, people with diabetes, cancer, impaired immune system, transplanted, and all people with immunocompromised weakness. Various studies have shown that three major events are respiratory disorders, lymphocytopenia, and cytokine storm as SARS-CoV-2 is transmitted through the ACE-2 receptor on the surface of alveolar type 2 lung cells; in which case, pneumonia, loss of lung function, acute respiratory distress syndrome (ARDS), shock and even death occur because of the failure in the adjustment of inflammatory responses from immune system and proliferation of cytokines. As the virus enters the cells, receptors of intrinsic immune system-TLR3, TLR7 (endosomal receptors) and RIG-I and MDA-5 (cytosolic receptors) detect the RNA of the virus. Involvement of the receptors ends up with the production of different types of cytokines such as type I interferons and inflammation. In respect of acquired cellular immune system of Th1, Th2, and Th17 lymphocytes with cytokine production, the lymphocytes T CD8+ (CTL) play their part by producing perforin, granzyme and cytokine. Humoral-acquired immune activity can be determined in most patients by producing IgM (9 days after disease onset) and IgG (two weeks after disease onset). SARS-CoV-2 makes use of mechanisms such as disruption in the production of type I interferons, reduction of MHC-I, MHC-II expression, and increase of Tim-3 and PD-1 expression on the surface of CTL cells (T cell exhaustion) in order to evade the immune system. In this paper, we present a review of the most recent data on the immunopathogenic mechanisms of the infection with respiratory viruses, especially SARS-CoV-2.