Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Ciliary Dysfunction Secondary to COVID-19. Explanation of the Pathogenesis From Analysis of Human Interactome With Sars-Cov-2 Proteome

Version 1 : Received: 24 December 2020 / Approved: 25 December 2020 / Online: 25 December 2020 (13:18:03 CET)

How to cite: Bermejo-Valdés, A.J.; Padrón-González, A.A.; Archer-Jiménez, J. Ciliary Dysfunction Secondary to COVID-19. Explanation of the Pathogenesis From Analysis of Human Interactome With Sars-Cov-2 Proteome. Preprints 2020, 2020120663 (doi: 10.20944/preprints202012.0663.v1). Bermejo-Valdés, A.J.; Padrón-González, A.A.; Archer-Jiménez, J. Ciliary Dysfunction Secondary to COVID-19. Explanation of the Pathogenesis From Analysis of Human Interactome With Sars-Cov-2 Proteome. Preprints 2020, 2020120663 (doi: 10.20944/preprints202012.0663.v1).

Abstract

Coronavirus Disease-2019 (COVID-19) is an infectious disease caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). There is sufficient experimental evidence to confirm that SARS-CoV-2 infection produces states of ciliary and flagellar dysfunction. However, these studies are unable to explain the observed effects molecularly, because they lack a sufficient understanding of the interaction between human proteins and virus proteins. Using the physical-chemical study of the human interactome in interaction with the SARS-CoV-2 proteome, we found evidence of interactions to explain the experimental effects from a molecular perspective. We found that ten viral proteins interact with key components in the maintenance of the molecular structure of axoneme. Additionally, we evaluated the pulmonary and extrapulmonary pathogenesis of COVID-19 from the point of view of ciliary dysfunction, and warned about other possible complications such as episodes of transient infertility that, due to the limitations of our work, would need verification.

Subject Areas

COVID-19; SARS-CoV-2; interactome; ciliary-flagellar dysfunction; infertility; pathogenicity

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