Capturing a Crucial 'Disorder-to-Order Transition' at the Heart of the Coronavirus Molecular Pathology-Triggered by Highly Persistent, Interchangeable Salt-Bridges.

ABSTRACT: The COVID-19 origin debate has greatly been influenced by genome comparison studies of late, revealing the emergence of the Furin-like cleavage site at the S1/S2 junction of the SARS-CoV-2 Spike (FLCS_Spike) containing its ₆₈₁PRRAR₆₈₅ motif, absent in other related respiratory viruses. Being the rate-limiting (i.e., the slowest) step, the host Furin cleavage is instrumental in the abrupt increase in transmissibility in COVID-19, compared to earlier onsets of respiratory viral diseases. In such a context, the current paper entraps a 'disorder-to-order transition' of the FLCS_Spike (concomitant to an entropy arrest) upon binding to Furin. The interaction clearly seems to be optimized for a more efficient proteolytic cleavage in SARS-CoV

SUBMITTER: Roy S 

PROVIDER: S-EPMC8875383 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature