  Smokers being witnessed with the mild adverse clinical symptoms of
SARS-CoV-2, the in-silico study is intended to explore the effect of nicotine
binding to the soluble angiotensin converting enzyme II (ACE2) receptor with or
without SARS-CoV-2 binding. Nicotine established a stable interaction with the
conserved amino acid residues: Asp382, Gly405, His378 and Tyr385 through His401
of the soluble ACE2 that seals its interaction with the INS1. Also, nicotine
binding has significantly reduced the affinity score of ACE2 with INS1 to -12.6
kcal/mol (versus -15.7 kcal/mol without nicotine) and the interface area to
1933.6 square Angstrom (versus 2057.3 square Angstrom without nicotine).
Nicotine exhibited a higher binding affinity score with ACE2-SARS-CoV-2 complex
with -6.33 kcal/mol (Vs -5.24 kcal/mol without SARS-CoV-2) and a lowered
inhibitory contant value of 22.95 micromolar (Vs 151.69 micromolar without
SARS-CoV). Eventhough ACE2 is not a potential receptor for nicotine binding in
the healthy people, in COVID19 patients, it may exhibit better binding affinity
with the ACE2 receptor. In overall, nicotines strong preference for
ACE2-SARS-CoV-2 complex might drastically reduce the SARS-CoV-2 virulence by
intervening the ACE2 conserved residues interaction with the spike (S1) protein
of SARS-CoV-2.
