The last century has seen two major pandemics caused 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, giving it 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 his graduate student Daphna Meroz, in collaboration with Dr. Tomer Hertz of Seattle's Fred Hutchinson Cancer Research Center, have developed 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 population. It may also lead to more precisely designed vaccines to combat these viral mutations.
Their method reveals that mutations in the virus' amino acids in specific positions, such as antigenic receptor sites, may explain how the new strain successfully spread throughout the population in 2009. These alterations allowed the strain to evade both existing vaccines and the immune system's defenses.
Playing a game of cat and mouse
Viruses and our immune systems are constantly at war. A virus constantly mutates to escape notice, and our immune system strives to play catch-up to recognize the virus and mobilize the body's defense system.
To determine the spread of the 2009 human pandemic flu, Prof. Ben-Tal and his fellow researchers analyzed the hemagglutinin protein, which controls the virus' ability to fuse to a host cell in the body and transfer the genome which contains the information needed to make more virus. Eventually, he says, our immune system is able to recognize a virus' hemagglutinin, w
|Contact: George Hunka|
American Friends of Tel Aviv University