Flu drug 'shows promise' in overcoming resistance
A new type of flu drug that can stop resistant strains in their tracks shows promise, say US researchers.
It permanently blocks a key enzyme on the surface of the flu virus, stopping it from spreading to other cells.
In mice it was found to effective against strains which were resistant to the two flu antivirals currently on the market, the journal Science reported.
The World Health Organization estimates that influenza affects three to five million people every year.
Resistance to the existing flu drugs Relenza and Tamiflu is becoming an increasing problem, largely due to their overuse.
The more exposure the flu virus has to the drugs - and in some countries it is available as a preventive treatment before people even catch the infection - the more chance it has of working out how to evade their effects.
Yet in the event of a flu pandemic they are the only weapon available for treating patients in the months before a vaccine can be developed.'Broken key'
A team of researchers from Canada, the UK and Australia developed a compound that binds to an enzyme on the surface of the flu virus called neuraminidase.
This enzyme is responsible for severing the connection between the flu virus and human cell so it can move on and infect other cells.
The new class of drugs - DFSAs - permanently bind to the enzyme, blocking its action and stopping it from spreading further, the journal Science reported.
Currently available antivirals also work by attaching to this enzyme.
But DFSAs do so in such a way that the flu virus cannot evolve to be resistant to the drug without rendering itself useless.
Tests in mice showed it works against both A and B influenza types and known resistant flu strains and researchers are now doing tests in other animals.
Study leader Prof Steve Withers from the University of British Columbia said: "Our drug agent uses the same approach as current flu treatments - by preventing neuraminidase from cutting its ties with the infected cell.
"But our agent latches onto this enzyme like a broken key, stuck in a lock, rendering it useless."
Co-author Dr Andrew Watts from the University of Bath said: "Our drug can work even better in drug resistant strains than in natural viruses emphasising that it is working through a totally different mechanism."
He added that realistically it would be six to seven years before the drug came to market.
Prof John Oxford, a virology expert at Queen Mary, University of London, said the work seemed to be a significant step forward.
"It is always nice to have an extra drug in the medicine cupboard and it would be reassuring if in the near future we had a second line drug."