ABSTRACT
SARS-CoV-2 is the coronavirus that originated in Wuhan in December 2019 and has spread globally. The observation of a low prevalence of smokers among hospitalized COVID-19 patients has led to the development of a hypothesis that nicotine could have protective effects by enhancing the cholinergic anti-inflammatory pathway. Based on clinical data and on modelling and docking experiments we have previously presented the potential interaction between SARS-CoV-2 Spike glycoprotein and nicotinic acetylcholine receptors (nAChRs), due to a “toxin-like” epitope on the Spike Glycoprotein, with homology to a sequence of a snake venom toxin. We here present that this epitope coincides with the well-described cryptic epitope for the human antibody CR3022 and with the epitope for the recently described COVA1-16 antibody. Both antibodies are recognizing neighboring epitopes, are not interfering with the ACE2 protein and are not able to inhibit SARS-CoV and SARS-CoV-2 infections. In this study we present the molecular complexes of both SARS-CoV and SARS-CoV-2 Spike Glycoproteins, at their open or closed conformations, with the molecular model of the human α7 nAChR. We found that the interface of all studied protein complexes involves a large part of the “toxin-like” sequences of SARS-CoV and SARS-CoV-2 Spike glycoproteins and toxin binding site of human α7 nAChR.
Competing Interest Statement
The authors have declared no competing interest.
Abbreviations
- aa
- Amino Acids
- ARDS
- Acute Respiratory Distress Syndrome
- ACE2
- Angiotensin Converting Enzyme 2
- COVID-19
- Corona Virus Disease 2019
- ECD
- Extracellular Domain
- LBD
- Ligand-binding domain
- nAChR
- Nicotinic Acetylcholine Receptor
- NCS
- Nicotinic Cholinergic System
- RBD
- Receptor Binding Domain
- SARS-CoV
- Severe Acute Respiratory Syndrome Coronavirus
- SARS-CoV-2
- Severe Acute Respiratory Syndrome Coronavirus 2.
