From Our 2009 Archives
Drug Impedes Body's Deadly Reaction to Flu Virus
Latest Cold and Flu News
FRIDAY, Jan. 23 (HealthDay News) -- A drug may be able to dampen part of the body's immune response so infections can be fought without a resulting overkill that may cause the person to perish, a new study says.
The compound sphingosine analog AAL-R, when administered directly into the lungs of mice, helped mitigate the cytokine response, a common immune reaction that can sometimes be so strong that it can harm as much as help, according to a report published in this week's issue of the Proceedings of the National Academy of Sciences. A severe "cytokine storm" can flood and clog the lung's alveoli with infection-fighting cells, making it so oxygen can no longer be properly absorbed by the body.
When administered to mice with the flu virus, the compound helped to temper the cytokine effect enough to prevent harm to the rodent while still allowing the body to fight the infection.
"Even though this compound does not kill the virus itself, the immunopathologic response was significantly impaired," study co-leader Dr. Michael Oldstone, of The Scripps Research Institute, said in a news release issued by the facility.
The researchers believe their findings may help prevent a much-feared pandemic of the H5N1 virus, more commonly known as bird flu, and the spreading of other deadly lung infections by helping make treatment more effective without harming the patient.
"We know that many of those who died in the 1918 influenza pandemic were young people, those with the strongest immune systems whose bodies mounted the strongest immunopathologic responses," Oldstone said. "Our hope is that our current research will yield answers about how to treat this kind of immune response not only in influenza, but also in other viral diseases such as hantavirus and SARS, in which pulmonary infiltration is severe."
They plan to study how sphingosine analog AAL-R receptors work and test combination therapy, such as adding Tamiflu to the compound, as a way to kill the virus while managing the immunopathologic response.
-- Kevin McKeever
SOURCE: The Scripps Research Institute, news release, Jan. 20, 2009
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