COVID-19 Immunogenetics and Immuno-Epidemiological Parameters
SARS-CoV-2 (COVID-19) infection has evolved to become a pandemic, in contrast to infections with SARS and MERS, whereas SARS-CoV-2 (COVID-19) has demonstrated having the similarities of genome sequence, receptor affinity, pathogenesis, and disease manifestation. Among the most severely affected patients, viral ribonucleic acid (RNA) has been detected in the plasma approximately 15% and viral detection in stool reveals possibility of fecal transmission. COVID-19 has been isolated in human saliva, nasopharynx and lower respiratory tract. Lacking lung biopsies or post-mortem sample investigations leads to an incomplete understanding of the pathogenesis of COVID-19 infection. The innate immune cells are born capable of producing T regulatory cell cytokine (interleukin (IL)-10 and T helper 17 (TH17) cell cytokines (IL-6 and IL-23), but inability of induction of T helper 1 (TH1) cell cytokines (type I interferons (IFNs), IFN-γ, and IL-12). A new lineage of oligoclonal T cells that express natural killer (NK)-related receptors (NKR) is formed, whereas the diversity of the T-cell receptor (TCR) repertoire decreased with age. In addition to the experimental evidence regarding the immunological features in neonates and children that are more prominent than in adults. In consideration of the pro-inflammatory response to the SARS-CoV infection, an overwhelming inflammatory reaction in aging population is a logical possibility. The mean age of COVID-19 patients is 52.4 years, whereas children and adolescents are the least likely group to be infected with the COVID-19, occurring in only 2 % of cases 19 years of age or younger. When the younger-age group get sick, they will get a mild form of COVID-19 without serious complications, with an average death rate of 0.2 %.