# 4719
Earlier today I wrote about the ICEID 2010 conference underway in Atlanta, and gave the link to the slide presentation abstracts.
While there are a great many presentations of note, one explores a theory I confess, I’d not heard before;
That nasal polyps and/or allergic rhinitis might make one more susceptible to contracting H5N1.
First the abstract, then a little discussion.
Enhanced Susceptibility of Nasal Polyp Tissues to Avian and Human Influenza Viruses
P. Auewarakul, O. Suptawiwat, P. Tantilipikorn, C. Boonarkart, P. Puthavathana; Mahidol
University, Bangkok, THAILAND
Background: Influenza viruses bind and infect respiratory epithelial cells through sialic acid on cell
surface. Differential preference to sialic acid types contributes to host- and tissue-tropism of avian and
seasonal influenza viruses.
Although the highly pathogenic avian influenza virus H5N1 can infect and cause severe diseases in humans, it is not efficient in infecting human upper respiratory tract. This is because of the scarcity of its receptor, 2,3-linked sialic acid, in human upper airway. Expression of sialic acid can be influenced by various factors including inflammatory process.
Allergic rhinitis and nasal polyp are common inflammatory conditions of nasal mucosa and may affect expression of the sialic acid and susceptibility to influenza infection.
Methods: To test this hypothesis, we detected 2,3- and 2,6-linked sialic acid in human nasal polyp and normal nasal mucosal tissues by lectin staining and infected explants of those tissues with avian influenza viruses H5N1 and seasonal influenza viruses.
Results: We show here that mucosal surface of nasal polyp expressed higher level of 2,3- and 2,6-linked sialic acid than normal nasal mucosa. Accordingly, nasal polyp tissues explants were more susceptible to both H5N1 avian influenza viruses and seasonal influenza viruses.
Our data suggest a role of nasal allergic conditions in susceptibility to influenza infection, especially by avian influenza viruses, which is generally
inefficient in infecting human upper airway.
Conclusions: The increased receptor expression may contribute to increased susceptibility in some individuals.
This may contribute to the gradual adaptation of the virus to human population.
Nasal polyps are small edematous grape-like sacs, filled with inflammatory cells and fluid, than can sometimes develop deep inside the nasal cavity.
They can appear singly or in clusters, and may come about as a result of long-standing inflammation, although often the cause is never known.
I’ll wait while everyone goes `eeewww’.
Ok, to continue.
In order to infect a host, a virus must attach itself to cells in the host’s body. Influenza viruses have an affinity for either the alpha 2,3 receptor cell or the alpha 2,6 receptor cell.
Avian adapted influenza viruses bind preferentially to Alpha 2,3 receptor cells, which are commonly found in the digestive tract of birds. This explains why most avian flu viruses are gastrointestinal infections in birds.
Human adapted viruses have an affinity for the alpha 2,6 receptor cell, which populate the upper airway and lungs. This is why influenza is a respiratory virus in humans.
There are some crossovers in receptor cells, and humans have some avian-like alpha 2,3 receptor cells, but most are deep in the lungs. It is harder for avian influenzas to reach those cells, but not impossible.
According to this research, however, inflammation processes – such as allergic rhinitis and nasal polyps – generate increased alpha 2,3 and alpha 2,6 receptor cells in the upper airway.
Which, theoretically anyway, could increase the odds of human acquisition of the H5N1 virus.
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