Swine flu patient .
(photo credit: Ariel Jerzolomiski)
The H1N1 influenza virus usually causes limited infection, but it occasionally
turns virulent and kills throughout the world.
Until now, scientists were
in the dark about what distinguishes the “swine flu” from the ordinary type in
pigs or seasonal outbreaks in humans – as in 1918 and 2009 – giving it the power
to travel extensively and infect large populations.
Prof. Nir Ben-Tal of
Tel Aviv University’s biochemistry and molecular biology department 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.
They just published their
research, which constitutes a valuable tool for identifying viral mutation
strategies, tracking various virus strains and developing vaccinations and
protective anti-virals. It appeared this week in the prestigious American
journal Proceedings of the National Academy of Science. They suggest their work
may also lead to more precisely designed vaccines to combat these viral
Their method reveals that mutations in the virus’s amino acids
in specific positions may explain how the new strain successfully spread
throughout the population in 2009, in which more than 18,000 died around the
world. 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,” said Ben-Tal. A virus constantly mutates to escape notice,
and our immune system strives to play catch-up and recognize the virus to
mobilize the body’s immune system.
To determine the spread of the 2009
flu, Ben-Tal and his colleagues analyzed the hemagglutinin protein, which
controls the virus’s ability to fuse to a host cell in the body and transfer the
genome, which contains the information needed to make more viruses. Eventually,
he says, our immune system is able to recognize a virus’s hemagglutinin, which
triggers its reaction to fight the virus.
Using a statistical algorithm,
the researchers compared amino acid positions in the 2009 strain of H1N1 against
the common flu and the strain of H1N1 found in the type affecting pigs. They
discovered major sequence changes had occurred, altering antigenic sites and
severely compromising the immune system’s ability to recognize and react to the
“Our new computation method showed the main differences between
the pandemic strain and the common seasonal H1N1 strain are in about 10 amino
acid positions,” Ben-Tal and Meroz reported. “That’s all it
Experiments conducted at St. Jude Children’s Research Hospital in
Memphis, Tennessee confirmed some of the theoretical predictions.
scientists believe that like the 1918 Spanish flu, which is estimated to have
killed at least 50 million people, the 2009 pandemic flu will likely go into
Now that this particular strain has been recognized by the
immune system, its power to infect has been compromised.
“But we were
lucky: despite the relatively low death toll of the pandemic in 2009, similar to
the number of deaths attributable to common seasonal flu, we might be facing
more dangerous future outbreaks of mutated H1N1 varieties.
Because of the
enormous mutation rate, viruses can spread widely and rapidly, and vaccines are
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 ability to
predict how a strain will morph and determine if a pandemic could strike.