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Comment by xel02 | Hacker News Reader

Different species have a different type from the protein family Hemagglutinin(HA)(they all look similar to each other) these proteins are similar to services offered on a port. Viruses like Influenza target HA but only of certain types. In the case of Influenza HA doesn't actually act as a port, its not designed to allow things to go into the cell, the virus however uses HA as a recognition marker for where it will attack.

As a side note H1N1 means HA type 1, and Neuraminidase (NA) type 1. NA is a necessary protein for Influenza to leave the cell after replication.

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Not entirely correct. Hemagglutinin is the protein on the virus coat. It binds to sialic acid on the surface of the cells. Sialic acids can have different glycosidic linkages. In humans, the predominant linkage type is alpha-1,6. In birds the predominant linkage is alpha-1,4. Pigs have a fairly even mix of both alpha-1,4 and alpha-1,6 which explains why they make good hosts for recombination.

I am under the impression that once a virus binds to a site, it attempts to push itself into the cell.

Would it be possible or practical to make a filter media, or throat spray using sialic acid to catch H1N1 viruses and fool them into 'thinking' they have reached a target location? The goal being to selectively trap or destroy as the virus attempts to enter a fake target cell. Could something like this help prevent infection or help to quell severe infections?

Would this be the computer analogous metaphor for a 'honey pot'.

Something in between a honey pot and a tarpit; which hopefully helps you develop your idea further because it sounds fascinating--from the perspective of me, with my no knowledge whatsoever of virology.

http://en.wikipedia.org/wiki/Tarpit_(networking)

Unfortunately, chemistry would thwart your efforts. The binding of proteins to other molecules (like sialic acid) is a reversible process. In other words, it's not as if each Hemaglutinin binds to a single sialic acid molecule and that's it. Each Hemaglutinin is constantly binding and unbinding, so adding extra sialic acid might slow down the process of fusing with the host cell, but it wouldn't prevent it.

Actually, the way that the current antivirals work is sort of the opposite. When the new viral particles are emerging from their host cell they end up stuck on the sialic acid molecules on the surface. That's where the Neuraminidase (the "N" of H1N1) comes in. It's job is to cut the new virus particles free of the host cell that produced them. If you block that, you can effectively stall the infection before it gets started.

There is something - mucus.

It doesn't fool them like you suggested, but rather it catches and tangles the viruses and physically prevents them from infecting a cell.

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