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October 6, 2005

1918 killer flu secrets revealed

Topics: Medicine

_39825355_virus_flu203.jpgScientists have worked out how the virus that caused the world's worst flu epidemic - infected man, and believe that the virus, which claimed the lives of up to 50 million people around the world, did indeed jump from birds to humans. Their work, published in Science, should help doctors identify at an earlier stage, just which future bird viruses pose a threat to man. However, the National Institute for Medical Research team warned that viruses cannot be stopped from crossing between species, and that the work is unlikely to aid the current fight against the current pandemic threat from avian flu in the Far East, since just knowing the structure of a virus is not enough to block its progress.

[...] The key first stage of infection is for the flu virus to attach itself to the cells in which it will breed.

It does this by using spike-like molecules called Hemagglutinins (HA) that bind to particular receptors on the surface of cells in the body.

Human and bird virus HAs interact with different cell receptors and therefore bird viruses do not usually infect humans.

However, the NIMR team has studied the HA of the 1918 virus in close detail, and found that only minor changes in its structure were required for it to start to bind with human cells as well as bird cells.

This gave it the ability to pass from birds to humans, and then between humans - with devastating results.

In related news, scientists in the US say they have recreated the 1918 Spanish influenza virus, and they have infected mice with it. They say the need to understand how flu viruses cause lethal pandemics outweighs any safety risks, however, those risks are both real and significant -especially in today's world of Islamic terrorism (obtaining the info via espionage and by simply reading scientific publications), which probably outweigh any concern for accidental release of the virus.

(...) By painstakingly piecing together viral fragments from hospital specimens and a victim buried in Alaskan permafrost, Jeff Taubenberger and colleagues at the US Armed Forces Institute of Pathology in Rockville, Maryland, have now sequenced all eight coding regions of the 1918 flu virus's genome. They published the last three - coding for the polymerase complex that allows the virus to replicate - on Wednesday (Nature DOI: 10.1038/nature04230).

(...) Meanwhile, Terrence Tumpey at the US Centers for Disease Control in Atlanta and colleagues used the sequences to rebuild the virus itself, and infect mice with it. They report this week that unlike other flu viruses, 1918 does not need a protein-splitting enzyme from its surroundings to replicate, instead using some hitherto-unknown mechanism. And as in 1918, it rapidly destroys lungs By replacing the genes for either the 1918 virus's surface protein, haemagglutinin (HA), or for its polymerase complex, with genes from a tamer, related flu, the team showed that both contribute to its deadliness, with the HA especially damaging for lungs.

(...) "This work will help us make vaccines and antivirals against pandemic strains," says Tumpey. It is unclear how, as the next pandemic is likely to be a different kind of flu.

(...) But, says Taubenberger, the 1918 sequences are already helping in another way: they prove that a bird flu can go pandemic without combining with a human flu, and suggest which mutations it needs. The most likely pandemic candidate, H5N1 bird flu, already has some of the mutations. We should watch out for more, he warns.

(...) The CDC handled the 1918 virus at only the second-highest level of biological containment, in which lab workers wear breathing hoods but not completely enclosed "spacesuits".

So have we come closer to finding a solution to an emerging H5N1 pandemic? Not really, we just have a little better understanding of the problem. Although H5N1 has no mutations giving resistance to the antiviral oseltamivir, so far, in studies published in July 2005, even high, prolonged doses of oseltamivir saved only 80 per cent of infected mice. If the drug has similar efficacy against 1918 flu, it might not stop the virus from spreading further if it escaped, and H5N1 can still mutate to acquire resistance to oseltamivir as it has already done with other antivirals(it is expected that amantadine and rimantadine will eventually lose their effectiveness against the influenza)

Related:
Bush may use troops, quarantine if bird flu breaks out: Doesn't he really mean WHEN it breaks out?

Pandemic Influenza - CIDRAP News Summary

US boosts medical stockpile for flu pandemic

Hat tip - Red Ink: Texas

Posted by Richard at October 6, 2005 12:40 PM



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