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Comparison of immune response to 1918 and H5N1 influeza viruses shows similarities

A comparison of the 1918 Spanish influenza and the H5N1 avian influenza viruses suggests that while the two viruses appear to trigger a similar abnormal immune response in animal models, there are distinct differences. Researchers from the University of Washington School of Medicine in Seattle report their findings today at the ASM Biodefense and Emerging Disease Research Meeting.

"The influenza pandemic of 1918-19 was responsible for at least 40 million deaths worldwide. Recent experiments in mouse and nonhuman primates have suggested a central role of the host immune response in 1918 and H5N1 disease severity," says John Kash, a lead researcher on the study.

Kash and his colleagues have previously published research on how the immune system responds to infection with the 1918 virus in mouse and nonhuman primate lungs, using bioinformatic tools to see what genes within the immune system are expressed in response to infection. They discovered that the virus caused an almost immediate and overwhelming immune system response that basically turned the immune systems of its victims against them.

In the current study, Kash and colleagues examined the gene expression in response to H5N1 avain influenza virus in mouse lungs and compared the immune response to the previously collected data on the 1918 influenza virus.

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"It looks like both these viruses elicit some sort of overblown inflammatory response. While at a fundamental level they look very similar to each other, there are subtle distinctions," says Kash.

In studying these commonalities and differences, Kash hopes to better understand how the viruses cause disease and hopefully develop new treatments. Eventually scientists may be able to develop drugs that could turn down or even switch off the unwanted activity while still allowing the immune system to combat the infection.

"What we are trying to do is understand the similarities and differences and what they mean. If we can understand those common mechanisms, we can better develop new treatments for the disease," says Kash.

Jim Sliwa | EurekAlert!
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