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1918 Flu Pandemic Virus Overwhelmed Lungs: Study

Jan. 18 (HealthDay News) -- An international team of scientists say they've uncovered an important clue as to why the 1918 Spanish flu virus was so lethal, killing over 50 million people worldwide.

Reporting in this week's Nature, the scientists say the virus caused an immune response that destroyed the lungs within a few days. It appears to disrupt the body's typical reaction to viral infection, causing the immune system to attack the respiratory system. As a result, victims' lungs fill with fluid, and they essentially drown.

The 1918 virus was the most deadly influenza strain in modern history.

A similar excessive immune system reaction has been noted in patients with the H5N1 avian flu virus, which has killed about 150 people worldwide. So far, the H5N1 virus has not developed the ability to spread easily among people.

The findings of study on the 1918 virus may lead to new ways to fight influenza and suggest that early intervention in patients may help prevent large death tolls in future outbreaks of highly pathogenic flu.

For this study, conducted at a government lab in Canada, scientists infected seven monkeys with a reconstructed 1918 virus. It was reconstructed using genes collected from the tissues of victims of the pandemic. Within 24 hours of being infected with the virus, the monkeys showed clinical signs of influenza. Within eight days, the monkeys were so sick that they had to be euthanized.

The rapid progression of the disease in the monkeys was similar to that noted in human victims of the 1918 outbreak.

The rapid growth of the virus in the monkeys after they were infected suggests that the virus somehow sets the stage for virulent infection, noted research team member Yoshihiro Kawaoka, a virologist at the University of Wisconsin-Madison.

"Somehow, early in infection, this virus does something to the host that allows it to grow really well. But we don't know what that is," Kawaoka said in a prepared statement.

By learning more about what's happening at the early stage of infection, scientists may be able to develop ways to halt the process, the researchers said.


SOURCE: University of Wisconsin-Madison, news release, Jan. 17, 2007
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