Flu is always a moving target for medicine because of its ability to reinvent itself to evade the body’s natural defences and vaccines and drugs.

Because the virus mutates at a high rate, the flu strains that circulate every winter are slightly different from those of the previous year. This process, called antigenic drift, requires the issue of fresh flu vaccines every year to protect against the latest strains.

It does not, however, carry a pandemic threat: the genetic changes involved are minor, so people who have already been exposed to flu generally retain a measure of immunity. New strains created this way can spread, and sometimes kill the young, old and infirm, but they do not sweep through entire populations.

What virologists fear is a different process, called antigenic shift or reassortment, which has driven previous pandemics. It is this that appears to have created the Mexican swine flu.

Antigenic shift allows flu to acquire much larger genetic changes very quickly, creating new strains to which the human immune system is entirely naive. These can make it much more dangerous because the body cannot immediately defend itself.

Flu mutates this way when two different strains infect the same host at the same time, which allows them to exchange whole sections of their genetic code.

A flu virus’s genome is split into eight segments, each of which is copied separately inside host cells, before being reassembled into daughter viruses and released to infect other cells. When two viruses are present their segments can get jumbled up, creating reassorted daughter viruses with genetic material from both strains.

“That is what appears to have happened here,” said Wendy Barclay, Professor of Influenza Virology at Imperial College, London. “From looking at the sequences, two viruses at least have come together.”

In the case of the swine flu the original strains appear both to have been pig viruses, which have swapped genetic material in an infected pig to create an entirely new strain that infects humans easily. Curiously, the new virus does not seem to cause disease in pigs. When the swine flu virus was identified as belonging to the H1N1 family it raised hope that humans might have some residual immunity to it, which might contain its pandemic potential. H1N1 viruses commonly infect humans and one was included in this year’s seasonal flu vaccine.

Genetic analysis, however, has now indicated that the H1N1 swine flu is too different from human H1N1 for previous vaccinations or flu infections to offer much protection.

“The homology [similarity] is very low, 70 per cent or less,” Professor Barclay said. “There is very little similarity, and you would expect there to be very little protection from antibodies to H1 human strains.

One encouraging discovery about swine flu is that analysis of its neuraminidase protein — the N of H1N1 — indicates that it should be sensitive to the antiviral drugs Tamiflu and Relenza, which target this protein. This bears out clinical experience so far, which suggests that patients respond well to the drugs.

However, Professor Barclay said that viruses with N1 neuraminidase were more likely than other strains to develop resistance to antivirals.

Peter Lachmann, Emeritus Professor of Immunology at the University of Cambridge, said: “Tamiflu resistance is extraordinarily widespread, and develops very quickly. We would be very lucky if this virus does not develop resistance.”

It remains unclear why the virus has killed so many young, healthy adults — a concern because this is characteristic of pandemic strains. One possibility is that the virus triggers a massive immune reaction called a cytokine storm, which is worse in fit people with a strong immune system.

This is thought to have been the chief cause of death during the Spanish Flu of 1918-19, which was caused by an H1N1 strain.

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