SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration

The post-infection of COVID-19 includes a myriad of neurologic symptoms including neurodegeneration. Protein aggregation in brain can be considered as one of the important reasons behind the neuro -degeneration. SARS-CoV-2 Spike S1 protein receptor binding domain (SARS-CoV-2 S1 RBD) binds to heparin and heparin binding proteins. Moreover, heparin binding accelerates the aggregation of the pathological amyloid proteins present in the brain. In this paper, we have shown that the SARS-CoV-2 S1 RBD binds to a number of aggregation-prone, heparin binding proteins including A13, a-synuclein, tau, prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 protein might assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain. The results will help us to prevent future outcomes of neurodegeneration by targeting this binding and aggregation process. (c) 2021 Elsevier Inc. All rights reserved.

Automated summary

Post-infection of COVID-19 can lead to a range of neurological symptoms, including neurodegeneration, which may be caused by protein aggregation in the brain. The interaction between SARS-CoV-2 Spike S1 protein receptor binding domain and heparin binding proteins could accelerate the aggregation of amyloid proteins in the brain, potentially leading to neurodegeneration. Targeting this binding and aggregation process could help prevent future outcomes of neurodegeneration.