Researchers have found that a gene mutation was the reason behind the increased virulence of the 2009 H1N1 swine flu virus which resulted in an unprecedented pandemic across the world.

The University of Wisconsin-Madison's School of Veterinary Medicine researchers identified the relocation of a specific amino acid in the gene matrix that enabled the 2009 H1N1 swine flu virus to hijack host cells, a feat that triggered the recent pandemic.

"We have found why the pandemic H1N1 virus replicated so well in humans," Yoshihiro Kawaoka, a leading influenza expert and a professor of pathobiological sciences at the University of Wisconsin-Madison's School of Veterinary Medicine, says in a press statement issued by the University.

Kawaoka believes that the 2009 H1N1 virus was a combination of four different avian and swine flu viruses that emerged over the past 90 years. The virus also included genetic residue of the 1918 pandemic virus that killed as many as 20 million people.

Typically, flu viruses require the presence of two amino acids -- lysine and asparagines -- in specific sites on a key avian protein in order to migrate from an animal host and replicate efficiently in human cells causing the disease.

But in the case of the 2009 H1N1 flu virus, the lysine amino acid was found located in a completely different location on the avian protein in the H1N1 virus. This is what gave the virus its ability to adapt to and co-opt human cells, the researchers say in their study published in the August 5 issue of PLoS Pathogens.

"This pandemic H1N1 has this mutation and is why it can replicate so well in humans. This gives us another marker to help predict the possibility of future flu pandemics," says Kawaoka.

According to the World Health Organization, as of July 25, 2010, the pandemic virus had caused more than 18,398 deaths worldwide.