Aids Research Spurs New Interest in Some Ancient Enemies

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The response to acute infection is also immediate. Like a fire, the incipient infection sets off alarms that alert the immune system to bring out its defensive weapons. It is an awesome arsenal. First, natural killer cells and the Pac-man-like macrophages rush to the scene to gobble up infected cells. After about a week, if this first-tier defense fails to control the threat, says Fields, "you bring out the guided missiles." These are antibodies -- produced by B cells upon the order of helper T cells -- that are custom-designed to home in on certain antigens, distinctively shaped proteins that characterize a particular type of virus, and destroy the enemy or render it harmless.

Although acute infections like influenza kill thousands each year, most people defeat their tiny attackers. Still, they may suffer while the battle is being waged. Indeed, many of the typical symptoms of infection -- fever, chills, itchy rashes, localized swelling -- are due less to the virus than to the vigorous activity of the immune system. However, once the body has created a population of antibody-producing B cells designed to combat a specific virus, immunity to that virus often lasts for decades, or even a lifetime. Then why does the common cold return again and again? One reason, scientists explain, is that colds can be caused by any one of hundreds of strains of bugs, most of them belonging to a group called the rhinovirus. A new cold can be brought on by a strain the immune system has not previously encountered.

Other viruses are responsible for longer-lasting effects. In so-called latent infections, the viral genes lie low, becoming active only intermittently, but throughout a lifetime. Herpes simplex (HSV), for example, makes its presence felt either in the form of genital lesions (usually caused by HSV-2) or as cold sores around the mouth (usually HSV-1), and comes under immediate attack by the immune system, which most of the time wins the battle.

But not the war. For between attacks, the latent herpes viruses hide out in the nerve centers, or ganglia. There they are so quiescent, expressing only five to ten of their 70 genes, that the immune system fails to detect them. Occasionally, for reasons that are poorly understood but that usually involve stress, fatigue, sexual activity and even sunburn, the immune system can no longer keep the hibernating viruses in check; they awaken, reproduce and head for the skin. "As long as the virus remains latent in the ganglia, it remains shielded," says Bernard Roizman, a leading herpes researcher at the University of Chicago. As a result, no permanent cure for herpes exists, and none is in sight.