In addition to relieving pain, fever, and inflammation, drugs such as aspirin somehow put the brakes on viruses. Now, scientists finally understand how. The drugs dampen a certain inflammatory enzyme, which also proves essential for replication of human cytomegalovirus (CMV). The finding could lead to new antiviral uses for old meds.
Aspirin and its cousins work by blocking production of cyclooxygenase (COX) enzymes. Newer drugs like Celebrex and Vioxx, which specifically block one of these enzymes, COX-2--and thereby avoid upset stomachs and other side-effects--are popular arthritis medications (they even outsell Viagra). Previous research showed that COX-2 inhibitors cut viral production in half in cultured cells, but how they did so was unclear. Researchers suspected that they halted the flow of prostaglandins--a family of inflaming compounds that aide viral replication.
The new study shows they were right. To find out how the drugs supress CMV, researchers led by Thomas Shenk of Princeton University and the University of Medicine and Dentistry of New Jersey in Newark infected cells with the virus, and then treated them with a COX-2 inhibitor. The drug reduced viral replication 1000-fold compared to drug-free control cells, the team reports in the 26 February online issue of the Proceedings of the National Academy of Sciences. Adding a prostaglandin compound to the drugged cells put viral replication back into full swing, although exactly why prostaglandin helps the virus remains a mystery.
But it's way too soon to start popping aspirin to fight the common cold, cautions Shenk. The experiment was on cultured cells, and the drugs were given at far higher doses than could be achieved in humans. But in theory, COX-2 inhibitors could be useful for fighting viruses besides CMV, says Kerry O'Banion, a neurobiologist at the University of Rochester in New York and part of the team that discovered the role of COX-2 in viral replication and holds a patent on its use.