Researchers reveal fibrin's critical role in COVID-19 by driving thromboinflammation and neuropathology, and highlight a potential antibody therapy to mitigate these effects.
By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Aug 29 2024 Uncovering the molecular interactions between fibrin and the SARS -CoV-2 spike protein , researchers pave the way for targeted therapies that could curb the devastating effects of long COVID.
Background Long COVID has become a significant public health concern, with coagulation and neurological complications arising during acute infection and persisting into the post-acute phase, contributing to morbidity and mortality. These issues affect patients across all age groups, including those with mild or breakthrough infections. Persistent and resistant blood clots, despite adequate anticoagulation, suggest underlying mechanisms that are not yet fully understood.
Fibrin polymerization in human plasma was assessed by measuring turbidity after initiating clotting with thrombin and calcium chloride. Scanning electron microscopy analyzed fibrin clots formed on silicon wafers, followed by image processing with National Institutes of Health Images. Study results Given the higher frequency and severity of abnormal blood clots in COVID-19 patients compared to other respiratory infections, it was hypothesized that SARS-CoV-2 might directly bind to fibrinogen, promoting clot formation and altering clot structure and function. A solid-phase binding assay confirmed the specific interaction between fibrinogen/fibrin and the SARS-CoV-2 spike protein, identifying key binding sites on both molecules.
Covid-19 ACE2 Antibody Blood Coronavirus Immune Response Immunotherapy In Vivo Inflammation Laboratory Mortality Protein Public Health Research Respiratory SARS SARS-Cov-2 Spike Protein
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