Using a technique known as reverse genetics, a team from University of Wisconsin-Madison were able to build a virus 93% similar to the 1918 Spanish flu by utilizing 8 genes found in recent avian flu strains.
The result was a flu virus more pathogenic than current avian flu strains, but less so than the Spanish Flu. The recreated strain was also not being transmitted between ferrets (a standard model for flu transmission) via respiratory droplets.
But not wanting to stop there the researchers, lead by Yoshihiro Kawaoka, began a number of experiments to determine the conditions under which their recreated version of the 1918 Spanish Flu could become transmittable between humans.
Their experiments identified 7 mutations in three of the viral genes that allowed the pathogen to become as infectious as the 1918 virus.
The conclusion of the study therefore became that the ingredients for a flu strain as deadly as the Spanish Flu strain of 1918 are already circulating in nature amongst domestic and wild birds.
The importance of the research is heavily stated by Kawaoka, who has come under fire from many scientists under the accusation that the sorts of experiments being carried out by Kawaoka and his team are putting the public at risk of a deadly flu pandemic should a virus escape from their lab.
Opponents, such as the previous scientific advisor to the UK government, Lord May, have labelled the study “extremely dangerous” and “absolutely crazy”. Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris has said that “”It’s madness, folly. It shows profound lack of respect for the collective decision-making process we’ve always shown in fighting infections. If society, the intelligent layperson, understood what was going on, they would say ‘What the F are you doing?”
But this research from Kawaoka and his team has revealed crucial information about the mutations that can occur in virus strains to make them more likely to infect mammals and increase the rate of transmission. One mutation for example has beeb identified as responsible for increased virus growth in mammals. By knowing what genes were involved in the 1918 pandemic, and the mutations likely to increase the deadliness of a flu virus, bodies such as the CDC will know what to look for when analysing seasonal flu strains, giving them more information when planning their response to flu each year.
Another interesting finding from the study is that people who have received the current US seasonal flu vaccine (protecting against the 2009 H1N1 virus) demonstrated some protection against the recreated 1918 strain, suggesting that if these genes were to combine and these mutations to take place, we would at least have some protection to begin with.
Find the paper from Cell Host and Microbe here.