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 %.