Good news! The inside of our noses where the Avian Flu would take hold are 32C, and in order for the Avian Flu to take hold our noses would have to be about the temperature of the gut of a bird - or 40C.
So unless there is a mutation - we are pretty much safe from the human to human spread of Avian Flu (or the start of a pandemic).
Want to know more? Here are some choice parts of the study I linked to above. Note that unless you're a scientist clicking on the link will give you a massive headache.
And before some of you nerdy hypersensitive dweebs cry fowl (get it, fowl?) that I copied directly from the study... This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. (Direct Link - http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000424)
Influenza type A viruses are endemic in aquatic birds but can cross the species barrier to infect the human respiratory tract. While transmission from birds to humans is rare, the introduction of novel avian influenza viruses into immunologically naïve human populations has significant pandemic potential. Avian influenza viruses are adapted for growth at 40°C, the temperature of the avian enteric tract. However, the human proximal airways, the likely site of initial inoculation by influenza viruses, are maintained at a cooler temperature (32°C), suggesting that zoonotic transmission may be limited by temperature differences between the two hosts. Using an in vitro model of human ciliated airway epithelium, we show that avian influenza viruses grow well at 37°C, a temperature reflective of distal airways, but are restricted for infection at 32°C. A panel of genetically manipulated human influenza viruses possessing avian or avian-like surface glycoproteins were also restricted at 32°C, but not 37°C, suggesting that avian virus glycoproteins are not adapted for efficient infection at the temperature of the proximal airways. Thus, avian influenza virus infection is restricted in the human proximal airways due to the cooler temperature of this region, thus limiting the likelihood of zoonotic and subsequent human-to-human transmission of these viruses.
Influenza viruses circulating in the human population are predominately type A and B, with type A being more common . All influenza type A viruses originate from aquatic birds and successful introduction of these avian viruses into the human population, by either direct adaptation or reassortment with already circulating human viruses, has led to influenza pandemics of historical significance (reviewed in –,). Still, documented evidence of transmission of avian influenza viruses directly from birds to humans is rare, partly because species barriers restrict avian influenza virus infection of the epithelial cells of the human respiratory tract, the primary site of influenza virus infection and spread.
Influenza A viruses possess a hemagglutinin (HA) attachment protein that binds sialic acid residues to facilitate infection of target epithelial cells. The HA of human influenza viruses preferentially binds to terminal sialic acid (SA) residues with α2,6 linkages, whereas avian influenza viruses preferentially bind to SA with α2,3 linkages –. The prevalence of α2,6 SA but paucity of α2,3 SA in the human respiratory tract has been considered to restrict infection by avian influenza viruses . Recent reports, however, have detected significant levels of α2,3 SA on human airway epithelium both in vitro and ex vivo, including in nasopharyngeal and tracheobronchial tissue –. This SA distribution also correlated with avian influenza virus infection in vitro and ex vivo and raised the possibility that avian viruses could infect the upper airways in vivo. Therefore, although it is universally accepted that human-to-human transmission of avian influenza viruses requires adaptation of HA to switch from α2,3 to α2,6 SA usage, the cumulative data published to date indicate that SA linkages and their respective distribution in the human airways are not the sole barrier to avian influenza virus infection –. Other host factors and viral genes are likely also important determinants of infectivity.
One such host factor that may limit zoonotic transmission is the difference in host temperatures between avian and human tissues that are susceptible to influenza virus infection. Avian influenza viruses are adapted for replication in the avian enteric tract at 40–41°C. While the surface temperatures of the human respiratory tract are variable, a temperature gradient clearly exists in which the surface temperature of the proximal large airways (i.e., nasal and tracheal) average 32+/−0.05°C while temperatures of the smaller, distal airways (i.e., bronchioles) are closer to that of the core body temperature, 37°C ,. While multiple transmission routes have been described for influenza viruses, the proximal airways likely represent a predominant site for human influenza virus inoculation as they provide a large exposed surface area of virus-susceptible epithelial cells . These cells are directly accessible by large droplet aerosols and by way of digital inoculation of the nasopharynx and conjunctival mucosa ,. Inefficient infection by avian influenza viruses, even in the presence of α2,3-linked SA, may be due to the cooler temperature of the proximal airways compared to that of the distal airways/lung regions where H5N1 avian influenza viruses appear to replicate efficiently .
Avian influenza viruses are attenuated at temperatures below 37°C and cold sensitivity of avian viral RNA replication in cell lines was linked to the presence of a glutamic acid at amino acid 627 in the avian virus polymerase subunit, PB2, instead of a lysine in the human virus PB2 . Lysine substitution at residue 627 of H5N1 viruses improved virus replication in mice . In addition to PB2, work utilizing human-avian reassortant viruses in MDCK cells provided initial evidence that avian glycoproteins, HA and neuraminidase (NA), may mediate temperature-dependent effects on viral growth . To our knowledge, other viral genes have not been well characterized, nor the HA and NA further evaluated, in their contribution to temperature sensitivity of avian influenza viruses.
To characterize the temperature dependency of avian vs. human influenza viruses in a relevant model of the target cell types of the human airways, we utilized an in vitro model of human ciliated airway epithelium (HAE). This model closely mimics the morphological and physiological features of the human airway epithelium in vivo and has been previously used to investigate infection by diverse respiratory viruses –. In humans, ciliated airway epithelium is present throughout the airways, extending from the nasal cavity and large proximal airways into the distal bronchiolar airway regions. Previously, we have shown that both human and avian influenza viruses replicate well in HAE and that human and avian influenza virus cell tropism correlates with the respective distribution of the specific sialic acid linkages . However, these previous studies were conducted at 37°C, reflecting conditions encountered in the distal airways . Others have also utilized these airway cell systems to characterize influenza virus replication of wild-type and recombinant viruses at 35°C ,,. In the present study, we utilize the HAE model, in combination with influenza virus reverse genetics, to investigate the influence of temperature on human and avian influenza virus infection, replication and spread. We demonstrate that, compared to human influenza viruses, avian influenza viruses are severely restricted for infection of human airway epithelium at the temperature of the human proximal airways. Then, using different strategies to ‘avianize’ human influenza viruses, we show that the temperature restriction of avian viruses is closely associated with the avian HA and NA glycoproteins.