Cascading from SARS-CoV-2 to Parkinson’s Disease through Protein-Protein Interactions

Extensive extrapulmonary damages in a dozen of organs/systems, including the central nervous system (CNS), are reported patients coronavirus disease 2019 (COVID-19). Three cases Parkinson’s (PD) have been as direct consequence COVID-19. In spite scarce data for establishing definitive link between COVID-19 and PD, some hypotheses proposed to explain reported. They, however, do not fit well with clinical findings patients, general, PD reported, particular. Given importance this potential connection, we present here molecular-level mechanistic hypothesis that explains these will serve explore CNS damage patients. The model explaining cascade effects from is developed by using bioinformatic tools. It includes post-translational modification host proteins lungs viral proteins, transport modified via exosomes out lungs, disruption protein-protein interaction proteins. Our supported finding 44 significantly expressed which associated whose interactions can be perturbed 24 lungs. These perturbators found interact form part cargoes human tissues. joint set PD-vulnerable tightly connected network more connections than expected selecting random cluster similar size proteome. presented provides several routes cascading PD. particular, autophagy/ubiquitination processes appears an important mechanism triggers generation large amounts containing their cargo, would insult potentially triggering Parkinsonism