Feb 25, 2002
NEW YORK - Certain pain relievers, including aspirin, might actually be able to fight some viruses instead of just treating virus symptoms such as fever, researchers report.
In a laboratory study, investigators in New Jersey have found that the group of pain relievers that inhibit an enzyme known as COX-2 prevent reproduction of a virus called human cytomegalovirus (CMV). This squelching effect, which can be accomplished by aspirin and other drugs, might very well apply to other viruses, according to an independent expert.
Even if the results apply only to CMV, the findings will be important if they're 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.
The effect of inhibition of COX-2 on CMV was first studied several years ago. A laboratory study showed that when muscle cells infected with CMV were treated with aspirin, the reproduction rate of the virus was cut in half.
The current study confirmed this result. When Dr. Thomas E. Shenk of Princeton University and colleagues infected skin cells with CMV, they found that inhibiting COX-2 reduced the virus reproduction rate more than 100-fold. The researchers used three experimental compounds in the study that specifically inhibit COX-2 alone. They also used another drug that is known to inhibit both COX-2 and COX-1, another type of enzyme. Traditional drugs such as aspirin and ibuprofen inhibit both enzymes, but a newer class of drugs, known as COX-2 inhibitors, are more targeted.
But the New Jersey team went further than the other researchers--they showed why inhibitors of COX-2 have this effect. They already knew that the drugs block the production of a naturally occurring chemical in the body called prostaglandin E2. This and other prostaglandins are responsible for the pain, fever and inflammation that develop in a wide range of disorders.
Shenk and his associates added to this knowledge by showing that prostaglandin E2 is vital to the reproduction of CMV. They added prostaglandin E2 to CMV-infected cells in which virus reproduction had been blocked by an inhibitor of COX-2. Prostaglandin E2 restored virus reproduction, the researchers report in the Proceedings of the National Academy of Sciences Early Edition, released online February 26.
There is evidence that prostaglandins play a role in the reproduction of other viruses, Dr. Edward Mocarski, Jr. of Stanford University suggests in a journal commentary. An example, he notes, is the herpes simplex virus. One strain of this virus causes cold sores and another causes genital herpes infections.
If scientists confirm that prostaglandins are involved in herpes and other viral infections, drugs that suppress prostaglandins might be "an auxiliary means of controlling infection," according to Mocarski.
SOURCE: Proceedings of the National
Academy of Sciences Early Edition 2002;10.1073/pnas052713799.
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