Research into 1918 virus can help bird flu fight
(Sep. 28, 2006) New insights into tackling the threat posed by bird flu have been made in a study into the 1918 flu pandemic, published today.
The outbreak of the 1918 virus - which was described as Spanish flu and is known to scientists as H1N1 - resulted in the deaths of up to 25 million people around the world.
Today's study, published in the science journal Nature, involved infecting mice with a recreation of the virus.
The results suggest the deaths were the result of an immune system overreaction. Previously, it had been believed that the scale of mortality in 1918 had been due to a second wave of infection that struck those already hit by flu.
However, the new findings indicate that deadly inflammation, triggered by an out of control immune response, could have been the real cause.
Researchers, led by Dr John Kash at the University of Washington, in Seattle, studied what happened to the lung cells of mice infected with the reconstructed virus.
Immune system genes were strongly activated, but the animals developed lung disease and died. Other mice infected with more benign flu viruses did not develop such a powerful immune response, and more of them survived.
"We think the host's inflammatory response is being highly activated by the virus, and that response is making the virus much more damaging to the host," Dr Kash said.
"The host's immune system may be overreacting and killing off too many cells, and that may be a key contributor to what makes this virus more pathogenic."
Scientists said the findings suggested that focusing on the immune system would be key to tackling the H5N1 bird flu virus.
Ordinary seasonal flu typically hits children, the elderly and those with weakened immune systems the hardest, but the 1918 virus infected many young and healthy adults.
Scientists have long questioned why the 1918 flu strain proved so deadly and why so many victims were people not normally vulnerable to flu.
Similar patterns of mortality have been observed in those infected by bird flu, although the virus has yet to develop into a disease that spreads from person to person.
Dr Christopher Basler, a co-author of the study from Mont Sinai School of Medicine, in New York, said the findings "could help us develop more targeted therapies to combat pathogenic infections, including different types of influenzas or perhaps avian influenza".
Professor Karl Nicholson, the professor of infectious diseases at the University of Leicester, said learning more about "the cause of the high morbidity of H1N1 ... might then open the way for alternative methods of treatment". (from www.guardian.co.uk)
(Sep. 28, 2006) New insights into tackling the threat posed by bird flu have been made in a study into the 1918 flu pandemic, published today.
The outbreak of the 1918 virus - which was described as Spanish flu and is known to scientists as H1N1 - resulted in the deaths of up to 25 million people around the world.
Today's study, published in the science journal Nature, involved infecting mice with a recreation of the virus.
The results suggest the deaths were the result of an immune system overreaction. Previously, it had been believed that the scale of mortality in 1918 had been due to a second wave of infection that struck those already hit by flu.
However, the new findings indicate that deadly inflammation, triggered by an out of control immune response, could have been the real cause.
Researchers, led by Dr John Kash at the University of Washington, in Seattle, studied what happened to the lung cells of mice infected with the reconstructed virus.
Immune system genes were strongly activated, but the animals developed lung disease and died. Other mice infected with more benign flu viruses did not develop such a powerful immune response, and more of them survived.
"We think the host's inflammatory response is being highly activated by the virus, and that response is making the virus much more damaging to the host," Dr Kash said.
"The host's immune system may be overreacting and killing off too many cells, and that may be a key contributor to what makes this virus more pathogenic."
Scientists said the findings suggested that focusing on the immune system would be key to tackling the H5N1 bird flu virus.
Ordinary seasonal flu typically hits children, the elderly and those with weakened immune systems the hardest, but the 1918 virus infected many young and healthy adults.
Scientists have long questioned why the 1918 flu strain proved so deadly and why so many victims were people not normally vulnerable to flu.
Similar patterns of mortality have been observed in those infected by bird flu, although the virus has yet to develop into a disease that spreads from person to person.
Dr Christopher Basler, a co-author of the study from Mont Sinai School of Medicine, in New York, said the findings "could help us develop more targeted therapies to combat pathogenic infections, including different types of influenzas or perhaps avian influenza".
Professor Karl Nicholson, the professor of infectious diseases at the University of Leicester, said learning more about "the cause of the high morbidity of H1N1 ... might then open the way for alternative methods of treatment". (from www.guardian.co.uk)
