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Multi-receptor mechanism and retinoid signaling disorder in the pathogenesis of COVID-19
Abstract
BackgroundMore than two years have passed since the pandemic and despite all the efforts of researchers, the pathogenesis of COVID-19 has not yet been resolved. Multisystem involvement, neuroendocrine involvement, and pathophysiological changes caused by SARS-CoV-2 in peripheral organs have been shown in many studies. However, the molecular mechanism of these pathophysiological changes caused by COVID-19 has not been elucidated. The frequent mutations of SARS-CoV-2 and the change in the interaction of the virus with host cells have further complicated the pathogenetic mechanism in COVID-19. Unfortunately, the mechanism determined at the beginning of the pandemic and based on the single receptor tropism of ACE2 was insufficient to explain the pathogenesis of COVID-19. It is known that SARS-CoV-2 causes retinoid signaling defects and chemosensory receptor disorders and exerts its pathogenic effects through these mechanisms. Multisystem involvement and different clinical presentations in COVID-19 suggest that virus-host interaction develops through multiple receptors and signaling pathways. The previous mechanism described via ACE2, based on single-receptor tropism, was insufficient to elucidate the pathogenesis of COVID-19 due to the absence of ACE2 receptors in most of the affected organs. In addition, there is no satisfactory explanation for the mechanism by which ACE2-free organs are affected in COVID-19. In this regard, we think that ACE2 is not a true binding receptor for the SARS-CoV-2 spike protein. With our recent molecular docking studies, STRA6 and its GPCRs were identified as new binding receptors of the SARS-CoV-2 spike protein. These studies have brought a multi-receptor mechanism to the pathogenesis of COVID-19. The multi-receptor mechanism clearly illuminates the complex pathogenesis of retinoid signaling disorder, systemic organ involvement, neuroendocrine involvement, loss of smell and taste, and many other peripheral symptoms and signs, which are considered an enigma in the pathogenesis of COVID-19. Therefore, we suggest retinoid signaling defect as the main pathogenetic disorder in COVID-19 and STRA6 and GPCRs as the main binding receptors of SARS-CoV-2 spike protein. This new mechanism also clarifies the changing symptoms and findings in COVID-19 with each new variant. In addition, these studies have revealed new signaling pathways and drug targets for the treatment and prophylaxis of COVID-19.
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Clown. You have no shame either. Didn't you say you were inspired by the articles I wrote earlier? You sent me the STRA6 article first, which I rewrote and edited. You added my name to the preprint version of this. Then you submitted the GPCR article, I wrote and edited it. You kept me busy, you didn't add my name to it. Then you submitted the 13-CIs retinoic acid study, which I rewrote and edited. After all this, I said that I would stone the studies with a compilation and analysis. I wrote the multi-receptor article from scratch to the dot myself. Here, I wrote about the relationship between STRA6 and GPCR receptors, which you found (perhaps stolen from elsewhere) by docking molecules, and retinoid signaling disorder. It is clear from the title of this article that I wrote it. Readers and editors will understand how similar the chosen words, accents, writing style, and style are to the articles I have written before. The articles are available in the WhatsApp records that I wrote and sent to you. I will share these with the editors.
It pains me that a work that I wrote with great effort was stolen from me and published under the name of a thief. I will definitely make you pay for this. You are so immoral to submit an article to five journals at once. You have no manners, no manners, no shame, and no morals. You're breaking all the code of ethics. You have no place in the scientific community. You are shameless, cheeky, and a thief.
Elkazzaz, M. (2022, February 23). Crosstalk among COVID-19, STRA6, Retinol, and G protein-coupled receptor may explain the novel hypothesis of Retinol depletion and retinoid signaling disorder of COVID-19 pathogenesis. https://doi.org/10.31219/osf.io/a6r3g
What a shame, man, are you crazy? This is my documented scientific discovery.This is a shame on you. You are doing something really disgraceful, as you are not young for such actions.
Mahmoud Elkazzaz, Tamer Haydara, Yousry Esam-Eldin Abo-Amer et al. STRA6 (vitamin A receptor), as a Novel binding receptor of COVID-19 (A breakthrough), 13 September 2021, PREPRINT (Version 3) available at Research Square [https://doi.org/10.21203/rs.3.rs-892203/v3]
https://www.researchsquare.com/article/rs-892203/v3
Mahmoud Ramadan Elkazzaz, Amr Ahmed, Tamer Haydara et al. Discovering of GPCRSs and GnRHRs as SARS-CoV-2 binding receptors, the Scientific Breakthrough that could explain the observed Hypogonadism, Hypothyroidism, Anosmia, Retinol deficiency, Neurological and Menstrual disturbance among SARS-COV-2 patients., 14 December 2021, PREPRINT (Version 2) available at Research Square [https://doi.org/10.21203/rs.3.rs-1155356/v2]
https://www.researchsquare.com/article/rs-1155356/v2
Mahmoud Elkazzaz, Amr Kamel Khalil Ahmed and Israa Mohamed Shamkh et al. STRA6 (vitamin A receptor), as a Novel binding receptor of COVID-19 . ScienceOpen Preprints. DOI: 10.14293/S2199-1006.1.SOR-.PP8LWHL.v1
Mahmoud Elkazzaz. Multi-receptor mechanism and retinoid signaling disorder in the pathogenesis of COVID-19. ScienceOpen Preprints. DOI: 10.14293/S2199-1006.1.SOR-.PPXLYQW.v1
https://www.scienceopen.com/hosted-document?doi=10.14293/S2199-1006.1.SOR-.PPXLYQW.v1