This preclinical study suggests the presence of a transmissible active agent from human rheumatoid arthritis synovium in mice.
No immediate implications for RA care; leaves open a possible transmissible agent and requires human validation.
The cause of rheumatoid arthritis is unknown.¹⁻⁴⁴The clinical aspects of this disease have suggested the possibility of an infection with a virus, bacteria, or other infectious agent as the cause of rheumatoid arthritis, yet no agent has been found. The development of the "slow-virus theory" and the reports of slow-virus diseases⁵with specific target organs have raised the possibility that rheumatoid arthritis also may be due to a slow virus. The triggering of acute exacerbations of inflammation by stress, the latency and periodicity, and its localization in the joints all suggest a specific etiologic agent, such as a slow virus. These reports influenced a series of experiments which were carried out over the past 18 months with Swiss Webster mice to determine whether an active agent could be transferred from the synovium of human patients with rheumatoid arthritis to mice. These experiments demonstrate the presence of an
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Stafford L. Warren (1969) studied this question.
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