Nat Med 2002 May;8(5):509-513
Levin MC, Lee SM, Kalume F, Jr FC, Hasty KA, Callaway JC, Zunt J, Desiderio DM, Stuart JM.
 Research Service, Veterans Affairs Medical Center, Memphis, Tennessee, USA  Center for the Neurobiology of Brain Disease, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA  Departments of Neurology, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA.
One hypothesis that couples infection with autoimmune disease is molecular mimicry
Molecular mimicry is characterized by an immune response to an environmental agent that cross-reacts with a host antigen, resulting in disease
This hypothesis has been implicated in the pathogenesis of diabetes, lupus and multiple sclerosis (MS)
There is limited direct evidence linking causative agents with pathogenic immune reactions in these diseases
Our study establishes a clear link between viral infection, autoimmunity and neurological disease in humans
As a model for molecular mimicry, we studied patients with human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a disease that can be indistinguishable from MS (refs. 5,6,7)
HAM/TSP patients develop antibodies to neurons
We hypothesized these antibodies would identify a central nervous system (CNS) autoantigen
Immunoglobulin G isolated from HAM/TSP patients identified heterogeneous nuclear ribonuclear protein-A1 (hnRNP-A1) as the autoantigen.
Antibodies to hnRNP-A1 cross-reacted with HTLV-1-tax, the immune response to which is associated with HAM/TSP (refs. 5,9)
.Immunoglobulin G specifically stained human Betz cells, whose axons are preferentially damaged.
Infusion of autoantibodies in brain sections inhibited neuronal firing, indicative of their pathogenic nature.
These data demonstrate the importance of molecular mimicry between an infecting agent and hnRNP-A1 in autoimmune disease of the CNS.