Immunological and Clinical Aspects of Immune Responses to SARS-CoV-2

The Coronavirus Disease 2019 (COVID-19) caused by a coronavirus named SARS-CoV-2 from the family Coronaviridae, was first reported in December 2019 in China. The disease have mild or severe symptoms such as fever, chills, cough, shortness of breath, body aches, and gastrointestinal symptoms, followed by severe inflammation, cytokine storm, acute respiratory distress syndrome, and dysfunction of other organs. In this narrative review study, the search was conducted on related studies published during January- October 2020 in Google Scholar, PubMed, Embase, and Scopus databases using the keywords Covid-19, Immunology, and Immunopathogenesis. Among abundant and mostly repetitive information, the immunological aspects were selected. The SARS-CoV-2 can enter the cell by binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor and Trans-Membrane Protease Serine 2 (TMPRSS2) on the surface of lung epithelial cells. The main pathogenic mechanism of infection with SARS-CoV-2 is the stimulation of inflammatory response followed by damage to the alveoli of lung tissue. In uncontrolled immune responses, the infiltration of macrophages, monocytes, neutrophils, and inflammatory T cells into the alveoli increases which leads to tissue damage in the lungs and other organs by overproduction of inflammatory cytokines such as Interleukin 6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF), Interleukin 6 (IL-8), Interferon gamma (IFNγ), etc. The Natural Killer (NK) and T cell dysfunction, lymphopenia, and infection of immune cells such as monocytes with ADE mechanism are factors causing the body’s failure in resistance to SARS-CoV-2 virus. Diagnosis of COVID-19 is based on the clinical symptoms and the results of molecular tests (e.g. Polymerase Chain Reaction test), or computerized tomography scan followed by serological tests and measuring biochemical factors in the blood (e.g. lymphocyte count, C-reactive protein, dimerized plasmin fragment D, etc.). Due to the association of the severity of COVID-19 with the uncontrolled immune response of the host, targeting any of the immunopathological pathways to inhibit inflammatory responses can be considered as potential therapeutic goals. The use of immune system regulators such as chloroquine, corticosteroids, inflammatory cytokine blockers such as anti-IL-6, anti-IL-1, and cell therapy at the right time have an enhanced effect on the recovery of the disease or inhibit the disease progression.