Herpesvirus linked to multiple sclerosis.

Compared to other babyhood diseases, roseola is mild. More than 9 out of 10 infants get it, running a fever, developing a rash, and usually recovering quickly.

Now, research shows that the herpesvirus that causes roseola can reemerge years later in people with multiple sclerosis, a nerve disease characterized by muscle weakness, vision problems, and paralysis. Some scientists suspect that this virus somehow triggers the disease.

Roughly 350,000 people in the United States have multiple sclerosis, which usually strikes between the ages of 20 and 40. It often begins as an off-and-on disease, with symptoms repeatedly appearing and disappearing. The disease eventually progresses to a downward spiral.

Many scientists believe that multiple sclerosis arises from a combination of factors that has not yet been established. Genetic makeup seems to predispose some people to the disease (SN: 9/16/95, p. 180). Researchers also suspect that it results from an autoimmune reaction in which the body's immune cells attack myelin, the sleeve of tissue that surrounds nerve cells. At sites in the brain where the myelin has been attacked, patients develop lesions--also called plaques or scleroses. Over time, many scleroses form, giving the disease its name.

Scientists don't know how the process starts, however. Suspecting that viruses play a role, several groups of researchers have investigated the herpesviruses in recent years. Some detected evidence of the roseola virus, or human herpesvirus 6 (HHV-6), in brain tissue taken from deceased multiple sclerosis patients.

In the first part of the new study, researchers at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., analyzed blood from 102 volunteers: 36 people with multiple sclerosis; 31 people with various other neurological diseases, including Parkinson's; 21 people with other inflammatory illnesses, such as lupus, which is also an autoimmune disease; and 14 healthy people. The researchers found antibodies to HHV-6 in two-thirds of multiple sclerosis patients in the recurrent stage of the disease.

Another test found that 15 of 50 multiple sclerosis patients harbored DNA from the replicating virus itself, says Steven Jacobson, a viral immunologist at the institute and a coauthor of the report, which appears in the December Nature Medicine.

Both findings were curious. First, the antibodies were the sort that a body produces in the throes of a battle against the virus, not "memory" antibodies that circulate routinely in the body, awaiting a call to action, Jacobson says. The only other study participants to show high concentrations of these antibodies were two of the patients with lupus and a patient with another inflammatory disease.

In the second part of the study, the researchers detected no active DNA from HHV-6 in anyone other than multiple sclerosis patients.

Preliminary evidence from an ongoing study shows that HHV-6 protein is present in areas of the brain where myelin is being destroyed--but not in healthy areas of the same patient's brain, Jacobson says.

"This is very interesting and potentially important work, but it leaves a conundrum," says David A. Hafler, an immunologist and neurologist at Harvard Medical School in Boston. "Is HHV-6 really involved [in the cause of multiple sclerosis], or is it just a consequence of the disease?" The evidence doesn't resolve this question, but the study adds to the growing school of thought among scientists that viruses are somehow involved with multiple sclerosis, Hafler says.

Jacobson agrees that no one knows what causes the debilitating disease, but he says that herpesviruses make fitting suspects. These viruses attack the nervous system and typically lie dormant for long stretches--just as multiple sclerosis does. "We know this is a latent and persistent virus," Jacobson says.

In any case, the findings convincingly show that many multiple sclerosis patients have an HHV-6 infection, says Byron H. Waksman, an immunologist at New York University.

The new study may provide evidence that HHV-6 acts to maintain, rather than cause, multiple sclerosis lesions, Waksman says. Either way, the long progression of multiple sclerosis may remain a puzzle even after the role of the virus is understood, he says.