The survival rate of mice infected with lethal amounts of H1N1 virus increased after a molecule was blocked, according to research published in Immunity.
Prohibiting a molecule increased the survival rates of mice infected with the H1N1 flu virus in research published April 10, 2014, by Immunity.
Researchers at McGill University in Canada inhibited a molecule called cyclooxygenase (COX) that allows ibuprofen and other non-steroidal anti-inflammatory drugs (NSAIDs) to lower a molecule called prostaglandin E2 (PGE2), which contributes to pain and fever.
“Drugs that specifically target PGE2 pathways have already been developed and tested in animals, so our results have excellent potential for clinical translation, not only for the treatment of influenza, but other viral respiratory infections that interact with similar host immune pathways,” senior author Maziar Divangahi said in a press release.
The mice in the study who were genetically engineered to lack PGE2 displayed enhanced immunity to the flu infection. When infected with a lethal dose of the virus, a majority of the mice without PGE2 survived. Additionally, mice treated with a PGE2 inhibitor compound showed enhanced antiviral immunity and produced better survival rates with a lethal dose of the fly virus compared to untreated mice.
“Previous studies produced conflicting results due to the inhibition of all prostanoids, not just PGE2,” Divangahi said. “Our findings suggest that different prostaglandins have different roles in antiviral immunity and that specific inhibition of PGE2 will be an effective therapy against influenza viral infection by boosting immune responses.”