Keywords: COVID-19, SARS-CoV-2, spike protein, lipopolysaccharide, TLR4, hyperinflammation
ReadPulmonary and systemic hyperinflammation are some of the prominent hallmarks of severe COVID-19 disease.
ReadThe COVID-19 pandemic has prompted a rapid response in vaccine and drug development. Herein, we modeled a complete membrane-embedded SARS-CoV-2 spike glycoprotein and used molecular dynamics simulations with benzene probes designed to enhance discovery of cryptic pockets.
ReadKeywords: SARS-CoV-2; Spike protein; allosteric drugs; allosteric effects of mutations; allostery; drug design; druggability; mutability.
ReadKeywords: SARS-CoV-2; Spike protein; allosteric drugs; allosteric effects of mutations; allostery; drug design; druggability; mutability.
ReadA central tenet in the design of vaccines is the display of native-like antigens in the elicitation of protective immunity. The abundance of N-linked glycans across the SARS-CoV-2 spike protein is a potential source of heterogeneity among the many different vaccine candidates under investigation.
ReadThe spike (S) protein is the main handle for SARS-CoV-2 to enter host cells via surface angiotensin-converting enzyme 2 (ACE2) receptors. How ACE2 binding activates proteolysis of S protein is unknown.
ReadThere is a link between high lipopolysaccharide (LPS) levels in the blood and the metabolic syndrome, and metabolic syndrome predisposes patients to severe COVID-19. Here, we define an interaction between SARS-CoV-2 spike (S) protein and LPS, leading to aggravated inflammation *in vitro* and *in vivo*. Native gel electrophoresis demonstrated that SARS-CoV-2 S protein binds to LPS.
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