Rheumatoid arthritis: review of searches for an infectious cause. Part I

No distinctive pattern has yet emerged from the accumulated mass of results that would provide a generally acceptable hypothesis of the etiology of rheumatoid arthritis. A number of immunologic aberrations have been described, but there has been no identification of a key immunologic defect that might link together the various components of the immune response into an agreed pattern. The possibility of a persistent antigenic stimulus arising from an infection cannot be confirmed or refuted. If a virus is involved, it would seem more likely to be a "slow" virus rather than a commonly recognized form, but there is no strong candidate of this type in view. Despite the fact that mycoplasmas are undoubtedly arthritogenic in other species, their role as an etiologic agent in rheumatoid arthritis has not been proven. The idea that bacterial cell wall peptidoglycan may provide a persistent stimulus has much to offer, but it is not possible at this stage to accept peptidoglycan as a recognized etiologic factor. This suggestion will, however, indoubtedly stimulate much further investigation.