In 2005, a group of American scientists resurrected one of history’s deadliest killer – the H1N1 flu virus of 1918 that killed approximately 50 million people worldwide. Using samples from a patient buried in Alaskan permafrost, they deciphered the virus’s genome and structure, rebuilt it from scratch and infected mice with it.

The move was understandably a controversial one. It has led to a greater understanding of the 1918 pandemic, and other important flu strains, but scientists have cited the possibility that this infamous killer could be accidentally released from a lab (as has happened before with other H1N1 strains). Worse still, it could be developed into a bioterror weapon. But according to Rafael Medina from the Mount Sinai School of Medicine, these worries may be unfounded. He has shown that since 1918, the world has gained an ally that will protect people against the deadly strain should it ever reemerge. That ally is a most unexpected one – the H1N1 swine flu virus from 2009.

The virus that went pandemic last year is actually a fourth-generation descendant of the 1918 virus. It’s part of a ‘pandemic era’ that was kicked off by the original strain and that has lasted for almost a century. Despite the 91-year gulf between them, the 1918 and 2009 viruses have some important similarities that set them apart from seasonal strains. This likeness means that antibodies that target one strain should work against the other. Indeed, elderly people who survived the 1918 pandemic still carry such defensive antibodies, and these can neutralise the 2009 virus too. This probably explains why elderly people, who are usually most at risk from flu viruses, were largely spared the brunt of the recent pandemic.

Now, Medina has found that the protection works the other way too, at least in mice. He gave mice the vaccine against the 2009 pandemic or antibody transfusions from humans who had themselves been vaccinated. Either way, the rodents produced antibodies that completely protected them against extremely lethal doses of the 1918 virus. Without the vaccine, all of the mice were dead within 8 days. With it, they barely showed any signs of illness and lost trivial amounts of weight. By contrast, vaccines against other strains of seasonal flu failed to provide any sort of protection against the 1918 monster.

Of course, this study has only looked at mice and Medina acknowledges that the next step will be to see if the 2009 vaccine will protect against 1918 flu in other animal models, such as guinea pigs, monkeys and ferrets. But for now, the results are encouraging

The 2009 pandemic spread worldwide and it is still the dominant strain of seasonal flu. Huge numbers of people were vaccinated when the pandemic hit, and the World Health Organisation has recommended that the standard annual flu vaccine should also target the pandemic strain. This means that large swathes of the population should now be immune to the 1918 virus should it ever rear its proteins again. It’s good news for scientist too; as Medina says, the current vaccine “should also serve as an additional layer of safety for researchers working with the 1918 influenza virus”.

Reference: Nature Communications http://dx.doi.org/10.1038/ncomms1026

More on flu:

• Flu survivors still immune after 90 years
• From Spanish to swine – how H1N1 kicked off a 91-year pandemic era
• How drug-resistant flu took us by surprise
• In a pandemic climate, public sneezing increases fears of unrelated risks
• Flu and Parkinson’s – how H5N1 bird flu causes neural degeneration in mice
• Origins of the swine flu pandemic