A flu virus which swept the globe and wiped out 20 million people in 1918 could soon be reconstructed following cutting-edge research in Oxford.

Highly-advanced technology designed by a top-level team of scientists, based at Oxford University's Sir William Dunn School of Pathology, means that scientists will soon have a better understanding of the deadly influenza virus.

They are currently concentrating on understanding the exact nature of the virus with a view to developing a highly-sophisticated vaccine within the next five years. Any attempts to recreate a strain of the virus of 80 years ago would have to be conducted under strictly monitored conditions in an air-locked laboratory to prevent the spread of the dangerous virus.

Scientists would have to wear protective clothing similar to space suits to shield them from succumbing to the deadly strain of the disease. However, there are currently no such facilities in Oxford for such an experiment.

The infectious respiratory disease kills thousands of people each year. The virus has a high mutation rate and stronger strains of the virus are developing all the time making people increasingly vulnerable. The aim behind reconstructing the 1918 virus would be to try to discover what made the so-called 'Spanish flu' so lethal. Historians say the 1918 outbreak was the most destructive in history, ranking with the Black Death as one of most serious epidemics of all time. It caused the death of 12,500,000 people in India four per cent of the country's population.

But scientists have so far been frustrated in their attempts to understand why it was so lethal because the virus was not isolated and preserved at the time.

Dr Ervin Fodor, a leading scientist in the Oxford University team, has been working for several years to develop a method for recreating old viruses from DNA molecules. The technique involves adding 12 rings, called plamids, of DNA to a cell in tissue culture which then produces a virus.

Dr Fodor believes that it is only once the virus is fully understood that scientists will be able to devise better protection against future flu outbreaks.

He says: "We are using this new technology in the development of vaccines. We particularly want to understand how the virus interacts with the host.

"This is a ground-breaking method and people have been trying for years to get to this stage.

"We still do not know why the 1918 virus was so deadly or why so many people died. Questions that have yet to be answered include whether there was something special about the virus, or whether people lacked immunity for some other reason. If we recreated that virus, under strict conditions, then we could understand why that virus was so deadly and then it would help us in the future to prevent something like this happening again." The current research programme has been funded by the Medical Research Council.

Dr Fodor's team is the only one outside the USA working on this specialised field of research.

Scientists based at the US Armed Forces Institute of Pathology, in Washington, have already completed years of vital research into the virus.

They have already worked out the sequence of two of the most important genes in the virus by using post-mortem material from the institute's archives.

They also took samples of RNA, similar to DNA, from a woman who died of the flu and was buried in Alaska, where the ground is frozen. Dr Fodor and his team are currently outlining the proposed research programme at the New Frontiers in Science exhibition at the Royal Society for Promoting Science, in London, this week.

Experts from across the country are aiming to help more people understand their work by taking part in the exhibition.

The Oxford team has developed interactive models which illustrate how the flu virus infects a host cell and also the processes they use to create new strains of the virus entirely from DNA molecules.

A second team from Oxford is also represented at the exhibition. They have outlined new techniques to study the development of amyloid plaques from proteins which may be one of the causes of Alzheimers' disease.