It is proposed that multiple sclerosis may be transmitted chiefly by sexual contact.

Arguments favouring this include: migration studies that suggest a transmissible agent in adolescence; clusters of multiple sclerosis which have occurred in low prevalence areas following entry of young males; the similarity of multiple sclerosis to tropical spastic paraplegia, a known sexually transmitted infection with resemblance to primary progressive multiple sclerosis; an increased rate in drug misusers; a similar age of onset and sex pattern to that found in sexually transmitted disease; increased incidence of multiple sclerosis in those using oral contraceptives; low multiple sclerosis rates in societies with a strict moral code; longitudinal shifts in sex prevalence that show an increase in women after the sexual revolution of the 1960s; and important exceptions to the worldwide distribution corresponding to countries with permissive attitudes to sex. Family, conjugal pair, twin, and adoption studies are compatible with an infectious cause of multiple sclerosis if this is sexually transmitted. It is not proposed that sexual transmission is the only cause but that inherited factors create a susceptibility to a sexually transmitted neurotropic agent. It is hoped this hypothesis might encourage a new direction of neurological research.

New study findings provide further evidence that infection with Epstein-Barr virus, which can cause mononucleosis, may increase the risk of developing multiple sclerosis (MS) later in life. Investigators discovered that people with the highest levels of antibodies linked to EpsteinBarr -- possibly indicating a history of severe infection -- were more than thirty times as likely to develop MS later in life than those with the fewest antibodies. These findings may one day help researchers solve the puzzle of why MS occurs, study author Dr. Alberto Ascherio of Harvard University in Boston told Reuters Health. But he cautioned that people who know they have been infected with Epstein-Barr -- even those who became very ill as a result - should "absolutely not" believe they are going to develop MS. Epstein-Barr is an extremely common type of herpesvirus, with more than 90 percent of the population in countries like the U.S. and U.K. estimated to have been infected at some point. The vast majority of people carry antibodies against Epstein-Barr in their bodies, Ascherio said, and only a small number develop MS. "All of us are infected (with Epstein-Barr), and only a few will get MS," he said. MS is a chronic disorder of the central nervous system in which the immune system, for unknown reasons, attacks the myelin sheath that insulates nerve fibers in the brain and spinal cord. Over time, the disease can lead to numbness, muscle weakness and stiffness, impaired vision and coordination problems. Most people become infected with Epstein-Barr during childhood, while others do so during adolescence or adulthood. Childhood infections often cause no symptoms. Among those with later infections, the virus can cause mononucleosis, or no symptoms at all. Mononucleosis, sometimes called the "kissing disease" because it can be spread by saliva, is characterized by fatigue, fever, swollen throat, and enlarged lymph nodes.

After infection with the virus, different people carry different levels of antibodies in their blood, with higher antibody levels possibly indicating a history of a strong immune system response to the virus. Previous research has shown that people with MS tend to carry higher levels of antibodies directed against Epstein-Barr virus. Whether the antibody increase precedes MS, however, has remained unclear. In the current study, reported in Wednesday's issue of the Journal of the American Medical Association, Ascherio and his colleagues examined blood samples collected between 1988 and 2000 from 83 people who later developed MS, and compared them with blood samples from 166 people without the condition. All of the people who developed MS carried antibodies against Epstein-Barr in their blood, as did 96 percent of those without MS. However, antibody levels at the study's start were consistently higher among those who later developed MS, the researchers found. On average, these people developed MS symptoms four years after their blood samples were taken -- suggesting there's a "long lag time" between Epstein-Barr infection and MS onset, according to the researchers. No one is sure why the immune systems of people with MS decide to launch an attack on their own tissue, Ascherio noted. Scientists have suspected that a combination of factors -including genetics and environmental "triggers" such as viruses -- may set off the aberrant attack. Since people with high levels of Epstein-Barr antibodies appear to be at higher risk, Ascherio speculated that some of the immune cells that become programmed to attack the virus may "cross-react" and begin to attack myelin as well. However, it's also possible that some other factor may cause the immune system to respond vigorously to Epstein-Barr and the body's own tissue. Ascherio said that a next step in this research may involve determining whether levels of antibodies against Epstein-Barr virus help diagnose MS earlier in people with symptoms of the disorder.