Sialic acids are super interesting, and the biosynthesis of sugars with them on is controlled by a small group of enzymes (20-ish). These enzymes have different tissues and cell type expression profiles, and can catalyse linkage of sialic acids in one of three conformations (linkages on carbons 3,6 and 8).
They’re in every cell, and the biosynthesis pathway limits how many different combinations of linkages you can make. So how exactly is it that these pathogens have often such amazing specificity for particular cellular receptors, if we know they bind sialic acids?
The answer lies in higher order assemblies called clustered saccharide patches, proposed by Varki a few decades ago. This is when the proteins (or lipids) that the sugars are found on have a particular shape, which enhances the binding by the pathogen (or Siglec). They were theoretical for a long time, but right now we have the tools to be able to dissect this, and our lab has had some success finding evidence for this, and we’re using our capabilities to dissect Siglec specificites too.
Also, I find it is massively unsatisfying that SARS-CoV 1/2 don’t use Sialic acids to recognise our cells, when it’s more likely than not to find a virus that binds sialic acids.
They’re in every cell, and the biosynthesis pathway limits how many different combinations of linkages you can make. So how exactly is it that these pathogens have often such amazing specificity for particular cellular receptors, if we know they bind sialic acids?
The answer lies in higher order assemblies called clustered saccharide patches, proposed by Varki a few decades ago. This is when the proteins (or lipids) that the sugars are found on have a particular shape, which enhances the binding by the pathogen (or Siglec). They were theoretical for a long time, but right now we have the tools to be able to dissect this, and our lab has had some success finding evidence for this, and we’re using our capabilities to dissect Siglec specificites too.