Out sick.
Pneumonia bacteria modified to shine show the amount of infection in the lungs of mice injected with an influenza virus containing a 1918 version of the PB1-F2 protein.
Jonathan McCullers / St. Jude Children's Research Hospital
Just in time for the flu season is the discovery that a single protein may explain much the unprecedented deadliness of the 1918 flu epidemic the discovery should help infectious disease experts spot future flu viruses that pose the greatest risk of causing a new global pandemic
1918 epidemic -. Also known as the Spanish flu - was the deadliest strain of the flu virus the world has ever seen ( science NOW, January 17). Estimates of deaths range 4-100000000. Some people have experienced the flu virus itself, but most of the deaths were due to pneumonia that people developed as a result of damage to their lungs. Why so deadly virus? Scientists suspect that a recently discovered protein called PB1-F2, which is found in many flu viruses, including the strain of H5N1 bird flu that killed 202 people, may hold answers.
To get a better handle on the role of PB1-F2 of the epidemic in 1918, a team led by Jonathan McCullers, a virologist at St. Jude Children's Hospital in Memphis, Tennessee, genetically modified a strain virus mouse influenza to produce a protein PB1-F2 identical to the strain of 1918. When the researchers dripped high doses of the modified virus into the noses of mice, all animals died within 8 days and had more lung inflammation than animals receiving similar doses of the same influenza virus with unaltered PB1-F2.
In a separate experiment, the researchers gave mice nonlethal doses of the modified flu virus and then infected with the bacteria causing pneumonia, Streptococcus pneumoniae . All animals died within 4 days and showed signs of severe pneumonia, the team reports in the October issue of Cell Host & Microbe . In contrast, 80% of mice that received the unmodified virus were alive 4 days after exposure to the bacteria of pneumonia and 20% were still alive when the study ended at 14 days.
"This is one of the big reasons 1918 was so bad, because PB1-F2 allowed bacteria to cause more problems due to lung inflammation and damage," McCullers said. How PB1-F2 amplifies flu virulence remains uncertain, but he says the protein could be a potential target for drugs against influenza, the aim being to delete it to help reduce lung damage and subsequent pneumonia.
Terrence Tumpey, a microbiologist with the Centers for Disease Control and Prevention in Atlanta, Georgia, said monitor protein PB1-F2 in flu viruses could help determine which ones pose the greatest threat to public health. "This could help us recognize whether a particular virus is something we have to watch," said Tumpey.
Related Sites
- The study
- influenza surveillance site of the World Health Organization
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