Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine
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BRIEF REPORT
Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine Darja Kanduc 1
&
Yehuda Shoenfeld 2,3
Received: 28 May 2020 / Accepted: 7 September 2020 / Published online: 18 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Introduction The ethiopathology of the diseasome induced by the SARSCoV-2 infection in the human host [1] is under intensive investigation. A likely mechanism is that the multitude of the diseases encompassed within COVID-19 derives from molecular mimicry phenomena between the virus and human proteins [2]. The rationale is that, following an infection, the immune responses raised against the pathogen can crossreact with human proteins that share peptide sequences (or structures) with the pathogen, in this way, leading to harmful autoimmune pathologies [3, 4]. Accordingly, lungs and airways dysfunctions associated with SARS-CoV-2 infection might be explained by the sharing of peptides between SARS-CoV-2 spike glycoprotein and alveolar lung surfactant proteins [2]. In support of this thesis, additional reports [5–8] highlight molecular mimicry and cross-reactivity as capable of explaining the SARS-CoV diseases. Of special interest, crossreactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2 has been also suggested [9]. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12026-020-09152-6) contains supplementary material, which is available to authorized users. * Darja Kanduc [email protected] Yehuda Shoenfeld [email protected] 1
Department of Biosciences, Biotechnologies, and Biopharmaceutics, University of Bari, Via Orabona 4, 70125 Bari, Italy
2
Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Aviv University School of Medicine, Tel-Hashomer, Israel
3
I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation, Sechenov University, Moscow, Russia
In this scientific framework, this study comparatively analyzed the peptide sharing between SARS-CoV-2 and mammalian species. Our reasoning is that if it were true that molecular mimicry between SARS-CoV-2 and human proteins contributes to or causes COVID-19, then different levels/ patterns of molecular mimicry vs. the virus should characterize the various animal species. Indeed, scarce data exist to indicate that domestic animals, for instances dogs and cats, can either transmit the virus or develop the virus-associated diseasome [10]. In general, currently, the consensus remains that there is no evidence that infected pets are a source of SARS-CoV-2 infection for people or other pets [11, 12]. Based on this rationale and using hexa- and heptapeptides as sequence probes [13–15], the peptide overlap between SARS-CoV-2 spike glycoprotein and mammalian proteomes was analyzed.
Methods Peptide sharing analyses have been extensively described elsewhere [16, 17]. Briefly, SARS-CoV-2 spike glycopr
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