For influenza (flu) viruses, hemagglutinin (HA) acts as the viral attachment protein by binds to host sialic acid-containing molecules as receptors. This provides abundant and ubiquitous sugars as receptors, but also binding to nonproductive receptors such as surfaces of dead cells. So influenza virus employs the neuraminidase to removes sialic acid, allowing the virus to be released after binding to sialic acid receptors that do not lead to viral infection. Severe cases of influenza virus infection by the new pandemic H1N1 virus correlate with specific HA mutations whereby efficient transmission in humans requires that its HA binds to sialic acid receptors in cells of the human upper respiratory tract. Macrophages normally keep infections out of the lower respiratory tract.

The NA's role in helping to release a budding flu viruses from infected host's cell after replication is very well known. However, that it is also implicated in such release from a dead cells prior to infection is new to me, although upon pondering it after a bit of reflection pretty intuitive too. I guess it won't be easy to distinguish the two (pre-infectious and post-infectious) types of NA's interactions experimentally, though?

But this is just a digression, so back to the original query - are there gene[s] already identified which govern development and types of possible viral target receptors on the surface of endothelial cells of human/mammals? And even more specifically, are there significant differences between receptors make-up between the lower and upper tract endothelia?

In connection with the previous question - what is the role of the sialic receptors on the endothelial cell surface, besides of course from providing a convenient binding sites for flu and other respiratory viruses?

As recently published by my Group (see my Publikation list: Anesthesiology 01/2013) The functional Promotor polymorphism -94ins/delATTG in the Gene of NFkB1 is a strong and Highly significant predictor of Death in septic patients and correlates with disease severity in ARDS patients including viral causes of ARDS. For further questions Do Not hesitate to contact me.

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@Simon, thanks - I'm trying to locate the full text PDF of that paper through resources available to me, but so far to no avail. Therefore the finer points and implications of what you wrote above are a bit elusive for the moment - hopefully not for too long :)