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Infection and multiple sclerosis—a new hypothesis?
  1. G J Stewart
  1. Institute for Immunology & Allergy Research, Westmead Millennium Institute, Westmead Campus, University of Sydney, Westmead NSW 2145, Australia; stewartg{at}westgate.wh.usyd.edu.au

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    Hypothesis of a sexually transmitted environmental component should be treated with care

    There is general agreement that multiple sclerosis is the result of both environmental and genetic factors. In the paper by Hawkes1 (this issue, pp 439–43) a hypothesis is proposed that the environmental component is an infectious agent, transmitted sexually. His thesis is based on a new look at old data; it has not been stimulated by recent discovery.

    Evidence for an environmental factor in multiple sclerosis has come from studies of migrating populations, small epidemics and variation of prevalence with latitude. Many of these studies are cited by Hawkes. The possibility that the environmental factor is a transmissible infection was reviewed in detail by Kurtzke2 in 1993, who proposed that the MS agent is an as yet unidentified retrovirus that results in widespread asymptomatic infection in early adolescence. Hawkes’ extension of the Kurtzke2 hypothesis to a sexually transmitted infection (STI) with a neurotropic agent appears to rely on his interpretation of the higher prevalence of MS in women, the low prevalence in native populations isolated from white males, a proposed correlation between sexual permissiveness and MS prevalence and with aspects of other diseases due to a known sexually transmissible agent, particularly HTLV-1.

    Whilst this succinct analysis and the accompanying table represent a scholarly and, in most parts, balanced effort, there are substantial difficulties with this hypothesis that can’t be overlooked. Adoption studies are not, as claimed, compatible with the STI hypothesis; the large Canadian MS adoptee study3 indicated that familial clustering is explained predominantly, if not exclusively, by genetic susceptibility. In the same population, there is convincing evidence that MS spouses are not at increased risk4 and some migration studies suggest an environmental factor acting well into adult years.5 Hawkes assumes close contact to mean sexual contact in the MS clusters without evidence. The explanation for the low MS prevalence in the isolated populations highlighted by Hawkes is more plausibly genetic. The lack of evidence for transmission of MS risk vertically, by breast milk, or blood transfusion represents a major difference between the epidemiology of MS and known retroviral infections such as HTLV-1 and HIV. The data cited with respect to drug use are not interpretable.

    There is also an issue of particular concern. People living with MS are often, fortunately, well connected to the world literature. The suggestions that susceptibility may be linked to sexual permissiveness or that childhood MS could result from child abuse have the potential to cause harm, unless it is made clear that they are pure speculation, based on interpretation of data collected for different purposes.

    Is the case, therefore, in support of an STI in MS aetiology sufficient to merit the case control studies needed to test this hypothesis? It would appear not, but readers will make their own judgements. A more prudent approach is perhaps to await the discovery of new infectious organisms, including STI, and to assess directly any relationship to MS as has occurred for HTLV-1, HIV, and other agents.

    Hypothesis of a sexually transmitted environmental component should be treated with care

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