The last century has seen two major pandemics brought on by the H1N1 virus “” the Spanish Flu in 1918 and 2009’s Swine Flu scare, which had thousands travelling with surgical masks and clamoring for vaccination. But scientists did not know what distinguished the Swine Flu from ordinary influenza in pigs or seasonal outbreaks in humans, passing on the power to travel extensively and infect large populations.
Until now. Prof. Nir Ben-Tal of Tel Aviv University’s Department of Biochemistry and Molecular Biology and the graduate student Daphna Meroz, in collaboration with Dr. Tomer Hertz of Seattle’s Fred Hutchinson Cancer Research Center, allow us a unique computational method to address this question. Published in the journal PNAS, the research presents a valuable tool for identifying viral mutation strategies, tracking various virus strains and developing vaccinations and anti-virals which can protect the populace. It may also result in more precisely designed vaccines to combat these viral mutations.
Their method reveals that mutations in the virus’ proteins in specific positions, such as antigenic receptor sites, may explain how the new strain successfully spread all through the populace in 2009. These alterations allowed the strain to evade both existing vaccines and the immune system’s defenses.
Viruses and our immune systems are constantly at war. The herpes virus constantly mutates to escape notice, and our immune system strives to play catch-up “” to recognize herpes and mobilize the body’s defense system.
To determine multiplication of the 2009 human pandemic flu, Prof. Ben-Tal and the fellow researchers analyzed the hemagglutinin protein, which controls the virus’ ability to fuse to some host cell in your body and transfer the genome which contains the data needed to make more virus. Eventually, he says, our immune system has the capacity to recognize a virus’ hemagglutinin, which triggers its reaction to fight against the virus.
Using a statistical learning algorithm, the researchers compared protein positions in the 2009 strain of H1N1 from the common flu and also the strain of H1N1 found in H1n1 virus, determined that major sequence changes which had occurred, altering antigenic sites and severely compromising the immune system’s ability to recognize and react to herpes.
“Our new computation method showed that the primary differences between the pandemic strain and the common seasonal H1N1 strain have been in some 10 amino acid positions,” Prof. Ben-Tal and Meroz report. “That’s what is needed.”
Experiments conducted by Sun-Woo Yoon, Dr. Mariette F. Ducatez and, Thomas P. Fabrizio from Prof. Richard J. Webby’s lab at St. Jude Children’s Research Hospital in Memphis, TN, confirmed some of the theoretical predictions.
Like its 1918 predecessor the Spanish Flu, this year’s pandemic flu will probably go into “hibernation” “” now that this specific strain continues to be identified by the immune system, its power to infect continues to be compromised. But we were lucky: regardless of the relatively low death toll of the pandemic in ’09, similar to the number of deaths due to common seasonal flu, we might be facing more dangerous future outbreaks of mutated H1N1 varieties.
Because of the enormous mutation rate, says Prof. Ben-Tal, viruses can spread widely and rapidly, and vaccines are fairly inefficient. In the future, a refined version of this computational method may ultimately be used to generically compare various strains of viruses. This in-depth analysis might lead to the opportunity to predict how a strain will morph and determine if your pandemic could strike.
This is an important step towards revealing the protein determinants of the emergence of flu pandemics, but there is more try to be achieved, they say.