A document by Amit K Maiti. Click on the document to view its contents.

SARS-CoV2 virus is believed to be originated from a closely related bat Coronavirus RaTG13 lineage after gaining insertions of RBD of spike (S) protein by exchanged recombination with pangolin virus Pan_SL_COV_GD. SARSCoV2 uses its entry-point key residues in S1 protein to attach with human ACE2 receptor. SARS-CoV2 evolution comprises any of these possibilities: it entered human from bat with its poorly developed entry-point residues much before its known appearance with slower mutation rate; or recently with efficiently developed entry-point residues having more infective power with higher mutation rate; or through an intermediate host. RaTG13 has 96.3% identity with SARS-CoV2 genome implying that it substituted ~1106 nucleotides to evolute as present-day virus. Temporal analysis of SARS-CoV2 genome from December 2019 shows that its nucleotide substitution rate is as low as 27nt/year with an evolutionary rate of 9x10-4 /site/year, which is a little less than other retrovirus (10-4 to 10-6 /site/year). Estimation of TMRCA of SARS-CoV2 from bat RaTG13 lineage appears to be in between 9-14 years. Furthermore, evolution of a critical entry-point residue Y493Q needs two substitutions with an intermediate virus carrying Y493H (Y>H>Q), although such an intermediate virus has not been identified in known twenty-nine bat CoV virus. Genetic codon analysis indicates that SARS-CoV2 evolution from RaTG13 lineage strictly follows neutral evolution with strong purifying selection whereas its propagation in human disobeys neutral evolution as nonsynonymous mutations surpasses synonymous mutations with the increase of ω (dn/ds) signifying its proceedings towards divergent selection predictably for its infection power to evade multiple organs.

SARS-COV2 virus is originated from a closely related  bat Coronavirus RaTG13 after gaining insertions by exchanged recombination with  pangolin virus Pan_SL_COV_GD. SARS-COV2 uses its entry-point key residues in S1  protein to attach with ACE2 receptor to infect human. The evolution of  SARS-COV2 could include any of these three possibilities: it entered human from  bat early with its poorly developed entry-point residues and remained silent  for long time with slower mutation rate to evade human immune system but  eventually perfected them for widespread infectivity; or recently with  efficiently developed entry-point residues having more infective power but  adapted  with higher mutation rate to  evade human immune system; or recently through an intermediate host having  human like conditions where it mutated both its entry-point residues as well as  immune evading system to survive easily in human. RaTG13 shows 96.3% identity  with SARS-COV2 genome of 29903 base implying that it substituted ~1106  nucleotides to become present-day virus. Using pairwise sequence analysis of  eighty-three SARS-COV2 genome from December, 2019, we show that its mutation  rate in human is as low as 36 nucleotides per year that would take  approximately 30 years to emerge as SARS-COV2 from bat RaTG13. Furthermore, a  critical entry-point residue 493Q that binds with K31 residue of ACE2  is evoluted from RaTG13 amino acid Y, which  needs the code must be mutated twice with an intermediate virus carrying amino  acid H (Y>H>Q). However, such an intermediate COV virus with 493H has not  been identified in bat or pangolin. Taken together, absence of any evidence of  silent presence of SARS-COV2  in human for  a long time or very high  mutation rate  or  an intermediate host or virus  emphasizes that either such an intermediate host or virus must be still obscure  in nature  or the emergence of SARS-COV2 is  urguably doubtful.