SARS-CoV-2 is a novel coronavirus, never encountered before by humans. Everybody is susceptible to infection, thus explaining the rapid viral spread and the Coronavirus disease 2019 (COVID-19) pandemics. The pathogenesis and possible treatment of COVID-19 requires in-depth knowledge of the immune-mediated mechanisms of the disease. We still need information on the cellular and molecular basis of the successful defensive reaction, whereas the role of dysregulated and excessive inflammation in aggravating the clinical picture has been described. In COVID-19, a condition of lymphopenia has been shown to correlate with the severity of clinical disease. Lymphopenia is caused by the reduction of T cells, both CD4+ and CD8+. Surviving T cells are functionally exhausted and reduced T cell counts may predict an unfavourable clinical course. In contrast, T cells able to react to SARS-CoV-2 peptides can be demonstrated in individuals, convalescent from mild and moderate disease. Antibodies to SARS-CoV-2 are produced in large amounts in patients with severe disease, two-three weeks after the occurrence of first symptoms. The kinetics of the antibody response to SARS-CoV-2 is not clearly defined, with IgG produced earlier or at the same time than IgM. The observation that patients with severe disease have the highest antibody levels has led to the suspicion that serum antibodies may be rather damaging than protective. At present, immunological studies suffer from limitations related to lack of information on asymptomatic individuals. In order to identify the pillars of the immune reaction triggered by COVID-19, we will compare the innate and adaptive immune populations in the peripheral blood of adults patients selected across the spectrum of disease severity ranging from SARS-CoV-2 positive asymptomatic individuals to patients with mild and severe COVID-19 over time to acquire knowledge on early immune responses and long-term immunity.
