A newly discovered gene that defends the body against flu could lead scientists to the first viral "antibiotic".
Drugs targeting the gene and others like it may in future provide broad spectrum protection against a range of potentially life-threatening virus infections, experts believe.
Currently no anti-viral treatment exists that mirrors the ability of antibiotics to clear away harmful bacteria. Antibiotics have absolutely no effect on viruses.
But new research suggests such medicines could become a reality in five to 10 years time.
Professor Paul Kellam, from the Wellcome Trust Sanger Institute in Hinxton, Cambridgeshire, said: "We'd like to think of it as an antibiotic but you have to think of it in a different way.
"The way broad spectrum antibiotics work is they target a common pathway that exists across different bacteria. This is turning the thing on its head so we're not so much looking at the diversity of viruses as the human cells they replicate in."
The gene, IFITM3 (interferon-inducible transmembrane 3), is found in every vertebrate species including bats, waterfowl and pigs - all of which can spread influenza viruses to humans.
A protein produced by the gene causes viral particles to become "trapped" in small membrane-bound bubbles in cells called endosomes. Unable to break out and inflict damage, the viruses within their endosomes are eventually eliminated from the cell by a natural "garbage disposal" system.
Scientists discovered that some individuals have a variant of the gene which stops the protein working properly, so they develop much worse flu symptoms and may even die.
An estimated 0.3% of the UK population have the variant, which increases their chances of a severe flu infection four to five times.
Some of the 0.1% of people who became seriously ill or died during the 2009 Swine Flu epidemic are thought to have fallen into this category.
Other work suggests the same gene may offer some protection against dengue fever, yellow fever and ebola - all serious viral infections.
"If there's one gene there are hopefully more," said Prof Kellam, speaking at the British Science Association taking place at the University of Bradford. "It raises the possibility of a whole spectrum of anti-viral genes that we can use to provide very good therapeutic targets."
IFITM3 belongs to a broad category of interferon stimulation genes, of which some 200 to 300 have already been identified, he said.
Many had variants that differed between species, indicating the kind of selection pressure that would be driven by viral infections.
The ultimate aim would be mimic the effects of the gene, for instance to reduce the severity of flu symptoms.