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http://www.nature.com/nsu/020819/020819-14.html

Deadly flu evades body's defences

Virus treats the immune system like "duck soup".
26 August 2002

JOHN WHITFIELD

 

Influenza can be a fatal infection.
© GettyImages

 

The lethal Hong Kong influenza is invisible to our body's immune defences, new research shows. The finding could help to identify future dangerous 'flu strains and perhaps explain why 'flu outbreaks of the past were so deadly1.

The strain in question, called H5N1, is immune to molecules called cytokines - the first line of defence against 'flu.

In 1997, H5N1 jumped from chickens to humans in Hong Kong. Eighteen people were hospitalized, six of whom died. Three million chickens were slaughtered to contain the virus, which can spread from birds to humans, but not between people.

"After infection with 'flu, cells start churning out cytokines," says virologist Robert Webster of St Jude Children's Research Hospital in Memphis, Tennessee. This triggers an immune response in uninfected cells, and suppresses most strains.

But to Hong Kong 'flu, cytokines "might as well be duck soup", says Webster - "it totally ignores them".

Simple but deadly

Just one genetic mutation lets H5N1 evade cytokines, Webster's team found. The researchers put the crucial gene into another form of 'flu; infected pigs became much sicker than those given the unmodified virus. The animals also remained infectious for longer.

Now the gene has been identified, it could be used to track down other threatening 'flu strains, says Albert Osterhaus, who studies 'flu at Erasmus University in Rotterdam, the Netherlands.

Quite how H5N1 sidesteps the immune system escape is not known. It may have other nasty tricks besides the changed gene, says Osterhaus. The effects of 'flu depend on the way that its eight genes interact, and that differs depending on the species it infects.

Back with a vengeance?

Hong Kong 'flu is similar to the strain that killed more than 20 million people in the 1918 'flu pandemic, Webster says. Both, for example, killed people in their mid-30s, who should have robust immune systems. They might share the immune-dodging ability, he thinks.

But there are also differences between the strains, says Alan Hay, a 'flu researcher at the National Institute for Medical Research in London. "It's a novel and very interesting finding," he says, but "it doesn't tell us anything" about the 1918 pandemic.

Influenza has been touted as a bioweapon, and the news about H5N1 could be used to produce a more deadly strain. It's always a possibility, says Webster, but 'flu is not the most obvious or easiest candidate for malicious use.

The threat we already face from the disease means that the benefits of the research outweigh the risk of new knowledge, Webster says. "We have to have this information. Sooner or later we're going to get a bad one, and by understanding the beast we've got a better chance of killing it."

 
References
  1. Seo, S. H., Hoffman, E. 7 Webster, R. G. Lethal H5N1 influenza viruses escape host anti-viral cytokine responses. Nature Medicine, Published online, doi:10.1038/nm757 (2002).

© Nature News Service / Macmillan Magazines Ltd 2002
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