Some Pain Relievers Help Prevent Viral Infections
By Biotechdaily staff writers
Posted on 21 May 2002
Pain relievers that reduce inflammation by preventing prostaglandin E2 synthesis through inhibition of the cyclo-oxgenase 2 (COX-2) enzyme may also help control or prevent viral infection.Posted on 21 May 2002
A study conducted on cytomegalovirus (CMV) growing in skin cell cultures has found that inhibition of COX-2 reduced the virus reproduction rate by more than 100-fold. Professor Thomas E. Shenk and colleagues from Princeton University (Princeton, NJ, USA) used three experimental compounds in the study that specifically inhibit COX-2 alone. They also used a drug that is known to inhibit both COX-2 and COX-1, another enzyme. Traditional drugs such as aspirin and ibuprofen inhibit both enzymes, but a newer class of drugs, known as COX-2 inhibitors, is more targeted.
The link between inhibition of prostaglandin synthesis and viral reproduction was confirmed when the researchers added prostaglandin E2 to cultures in which virus reproduction had been blocked by an inhibitor of COX-2. The added prostaglandin restored virus reproduction to its previous level.
This study, reported in the Proceedings of the National Academy of Sciences Early Edition, released online February 26, 2002, was focused on CMV growing in tissue culture. However, the findings will be important if they are confirmed by clinical studies. CMV infects most adults without causing illness, but it can be deadly in people with weak immune systems, such as AIDS patients. Also, CMV infection in pregnant women is a leading cause of birth defects, especially hearing impairments.
In a journal commentary, Dr. Edward Mocarski, Jr., of Stanford University (Stanford, CA, USA) pointed out that there is evidence that prostaglandins play a role in the reproduction of other viruses, such as the herpes simplex virus, which causes cold sores and genital herpes infection. If clinical studies confirm the relationship between prostaglandins and virus reproduction, drugs that inhibit prostaglandin synthesis may become an important means of controlling infection.