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.