Is multiple sclerosis an age-dependent host response to measles?

A hypothesis is presented that multiple sclerosis (MS) may represent an unusual host response to measles virus, dependent upon when the measles virus is acquired. If acquired late in childhood or near adolescence, the risk of MS is increased. Evidence to support this hypothesis is still meager, but there is ample support from many types of infection for the idea that a host's response may vary with age at the time of infection. As measles virus titers are somewhat increased in MS, evidence for age-dependent alteration in host responsiveness to measles may be taken as further support for the hypothesis. In addition, epidemiologic and clinical data linking MS frequency and average age at the time of measles infection exist. In those areas where MS is rare, measles tends to occur early in life; where MS is common, measles tends to occur later. In case-control studies, measles occurred later in MS patients than in the control groups. Finally mechanisms which might explain an age-dependent alteration in host responsiveness were considered, including maturation of an immune system or maturation of a CNS target cell, e.g. the oligocyte. Additional studies are needed to establish a firmer basis for the concept that risk of MS might be determined, in part, by the age at which a certain infection (e.g. measles) is acquired. If the hypothesis is correct, the mass measles vaccination programs should start to produce a decline in MS frequency. Because the event causing MS is believed to occur before age 15 and MS begins on the average by age 30, a 15-year lag in the effect of measles vaccine on MS frequency is to be expected. Mass measles vaccination was began in 1965, thus by 1980, a decline in MS frequency might be looked for as a test of the hypothesis. Perhaps by the V Pan-American Congress of Neurology, we shall be able to report that MS is disappearing.