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Human nose too cold for bird flu, says new study

Shiloh

Editor, Senior Moderator
Source: http://www.eurekalert.org/pub_releases/2009-05/icl-hnt051409.php

Public release date: 14-May-2009

Contact: Lucy Goodchild
lucy.goodchild@imperial.ac.uk
44-207-594-6702
Imperial College London
Human nose too cold for bird flu, says new study

Avian influenza viruses do not thrive in humans because the temperature inside a person's nose is too low, according to research published today in the journal PLoS Pathogens. The authors of the study, from Imperial College London and the University of North Carolina, say this may be one of the reasons why bird flu viruses do not cause pandemics in humans easily.

There are 16 subtypes of avian influenza and some can mutate into forms that can infect humans, by swapping proteins on their surface with proteins from human influenza viruses.

Today's study shows that normal avian influenza viruses do not spread extensively in cells at 32 degrees Celsius, the temperature inside the human nose. The researchers say this is probably because the viruses usually infect the guts of birds, which are warmer, at 40 degrees Celsius. This means that avian flu viruses that have not mutated are less likely to infect people, because the first site of infection in humans is usually the nose. If a normal avian flu virus infected a human nose, the virus would not be able to grow and spread between cells, so it would be less likely to damage cells and cause respiratory illness.

The researchers also found that when they created a mutated human influenza virus by adding a protein from the surface of an avian influenza virus, this mutated virus struggled to thrive at 32 degrees Celsius. This suggests that if a new human influenza strain evolved by adopting proteins from an avian influenza virus, this would need to undergo further changes in order to adapt to the conditions in the human body.

The researchers reached their conclusions by growing cells from the human airway and infecting them with different human and avian influenza viruses, including H5N1, to see how well the viruses grew and spread. The human influenza viruses grew equally well in the cells whether they were maintained at 37 degrees Celsius, our core body temperature, or at 32 degrees Celsius, the temperature of the nose. In contrast, the four avian influenza viruses tested grew well at 37 degrees Celsius but grew very slowly at 32 degrees Celsius.

When the researchers added proteins from an avian influenza virus to a human influenza virus, the human influenza virus also grew slowly and struggled to replicate at 32 degrees Celsius.

As viruses kill the cells they infect, the researchers also measured the extent of cell death in the model. This showed that at 32 degrees Celsius, far fewer cells died as a result of infection with avian influenza compared with human influenza, supporting the idea that the avian virus could not thrive at that temperature.

Professor Wendy Barclay, one of the authors of the study from the Division of Investigative Science at Imperial College London, said: "Bird viruses are out there all the time but they can only cause pandemics when they undergo certain changes. Our study gives vital clues about what kinds of changes would be needed in order for them to mutate and infect humans, potentially helping us to identify which viruses could lead to a pandemic.

"It would be impossible to develop vaccines against all 16 subtypes of avian flu, so we need to prioritise. By studying a range of different viruses in systems like this one we can look for warnings that they are already beginning to make the kinds of genetic changes in nature that mean they could be poised to jump into humans; animal viruses that spread well at low temperatures in these cultures could be more likely to cause the next pandemic than those which are restricted," added Professor Barclay.

###

The research was funded by the Medical Research Council in the UK and by the NIH in the USA.
 
Re: Human nose too cold for bird flu, says new study

Commentary

Swine H1N1 Outpaces Seasonal Flu In the United States
Recombinomics Commentary 21:51
May 12, 2009


The week 17 CDC report on seasonal flu in the United States was striking. The normal bell shaped curve of cases detected by CDC sentinel labs was suddenly interrupted by a sharp spike. Although the height of the spike was driven somewhat by increased surveillance due to the detection of H1N1 swine, the composition of the bar representing week 17 was a clear signal that swine H1N1 had taken change of influenza cases in the US. The initial data for influenza had 334 and 300 positives for H1 and H3, respectively, but there were 326 and 304 isolates for swine H1N1 or untypable influenza A (which is swine H1N1 that has not yet been confirmed). The updated data posted this week was even more striking, with 370 and 342 isolates for H1 and H3 respectively, while swine H1N1 and untypable influenza A were 524 and 259. Thus, there was more swine H1N1 than the combination of H1 and H3 seasonal flu.

The spike in H1N1 swine cases created a backlog at the CDC, which could be seen in a map of confirmed and probable cases (see US map). The confirmatory testing was handed off to the state labs to eliminate the backlog, but soon state labs were acknowledging that the samples tested were the tip a very large iceberg, and future testing would target more serious cases.

This movement of swine H1N1 into the human population is cause for concern. The increase over seasonal flu may be driven by the avian PB2 gene in the swine isolate. Position 627 is E, which favors growth at the higher body temperature of birds. Seasonal flu has a K at position 627, which allows for more rapid replication at a lower temperature, which is consistent with the internal temperature of a human nose in the winter.

The presence of avian PB2 may offer a selective advantage over the summer, when seasonal flu falls to barely detectable levels. However, the swine H1N1 that moves south in the upcoming months will be growing under colder conditions, which may favor the acquisition of E627K though reassortment or recombination. This change could create a more virulent H1N1 in the fall in the northern hemisphere.

Thus, the swine H1N1 may be launching a two virus strategy. The H1N1 with avian PB2 will dominate in the northern hemisphere over the summer, while the H1N1 in the southern hemisphere will acquire E627K and establish dominance during the winter months.

Thus, the spread of H1N1 is in high gear, as WHO debates if a swine H1N1 is a swine H1N1 and if a pandemic at phase 6 is really at phase 6.

Swine H1N1 doesn't read WHO press releases.

It just gains transmission efficiencies via homologous recombination.
(Emphasis mine)

http://www.recombinomics.com/News/05120903/Swine_H1N1_Seasonal.html

It's nice that other researchers have arrived at a conclusion that Niman, and many long-term flubies reached years ago.
 
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