Re: On the future of flu vaccine and anti-viral usage
Yes you are right the sialic acid residues in the mucus are going to imped the virions progress to the cell but there is no particular time constraint in that the NAs can keep cleaving the bonds until the HA binding site finds a residue on a cell and start endocytosis (assuming the delay did not put it in the path of a macrophage). The presence of NAIs would inactivate some of the NAs and slow its progress further. The situation at budding would be slightly different in that a failure to make a quick escape would leave the virus open to either being dragged back into the dying cell or being destroyed by the white blood cells which would have been attracted by the cytokines released during its forming cell's apoptosis.
This may be what you are referring to, if so you have a good memory as it was 4 years ago. Link to the post from which this was part of the comments.
Re. the mucusJJackson ? 4 years ago If I understand correctly the Neuraminidase prunes sialic acid residues from glycoproteins. This is useful in allowing a clean get away after budding and also to stop binding of virions to each other. How does the virus prevent its NAs from removing the residues it needs to bind onto the glycocaylx before fusion? Wouldn?t its NAs be freeing it as fast as it could bind?
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profvrr Mod JJackson ? 4 years ago Always an interesting question. The idea is that during entry, the HA
binds and the particle enters before the slower-acting NA can remove
the sialic acid. This idea has some support from the HA assay;
initially virions bind red blood cells but after approximately 30
minutes the NA cleaves off sialic acid and reverses the HA. See
http://www.virology.ws/2009/05....
JJackson profvrr ? 4 years ago Thanks but that then begs the question why when a new virion is budded does it not immediately bind and restart the fusion process before the NAs cut it free. On both occasions you have a virion adjacent to cell what is the difference why is there a net benefit to having NA cleaving sialic resisdues? There obviously is one or neuraminidase inhibitors would not work. I saw this http://www.ncbi.nlm.nih.gov/pu... and assumed it was due to nuraminidase having an inhibitory effect on cell infection although that effect was significantly outweighed by the benefits when budding
profvrr Mod JJackson ? 4 years ago The NA protein is inserted into the plasma membrane before the virion
buds from the surface. Its presence may lead to removal of sialic
acids, which would prevent re-binding of the newly synthesized
particle. In theory at least; there are no data that directly answer
your question. The results in the paper you cite are consistent with
the idea that NA has some inhibitory effect during infection as would
be expected. Clearly there are significant differences between
infection and budding that are not fully understood.
Yes you are right the sialic acid residues in the mucus are going to imped the virions progress to the cell but there is no particular time constraint in that the NAs can keep cleaving the bonds until the HA binding site finds a residue on a cell and start endocytosis (assuming the delay did not put it in the path of a macrophage). The presence of NAIs would inactivate some of the NAs and slow its progress further. The situation at budding would be slightly different in that a failure to make a quick escape would leave the virus open to either being dragged back into the dying cell or being destroyed by the white blood cells which would have been attracted by the cytokines released during its forming cell's apoptosis.
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