Abstract
Viruses share antigenic sites with normal host cell components, a phenomenon known as molecular mimicry. It has long been suggested that viral infections might trigger an autoimmune response by several mechanisms including molecular mimicry. More than 600 antiviral monoclonal antibodies generated against 11 different viruses have been reported to react with 3.5% of cells specific for uninfected mouse organs. The main pathological feature of tropical spastic paraparesis/human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (TSP/HAM) is a chronic inflammation of the spinal cord characterized by perivascular cuffing of mononuclear cells accompanied by parenchymal lymphocytic infiltration. We detected the presence of autoantibodies against a 98- to 100-kDa protein of in vitro cultured human astrocytes and a 33- to 35-kDa protein from normal human brain in the serum of HTLV-I-seropositive individuals. The two cell proteins exhibited molecular mimicry with HTLV-I gag and tax proteins in TSP/HAM patients, respectively. Furthermore, the location of 33- to 35-kDa protein cross-reaction correlated with the anatomical spinal cord areas (in the rat model) in which axonal damage has been reported in several cases of TSP/HAM patients. Our experimental evidence strongly suggests that the demyelinating process occurring in TSP/HAM may be mediated by molecular mimicry between domains of some viral proteins and normal cellular targets of the spinal cord sections involved in the neurodegeneration.
Highlights
Viruses that share antigenic sites with normal host cell components are part of a phenomenon known as molecular mimicry [1]
immunoglobulin G (IgG) antibodies against a 98- to 100-kDa astrocyte protein were detected in the sera of 100% (11/11) TSP/HAM patients included in the study
Recent studies have revisited the molecular mimicry with proteins of human T-lymphotropic virus type I (HTLV-I) as a process that may play some role in the progression of TSP/HAM
Summary
Viruses that share antigenic sites with normal host cell components are part of a phenomenon known as molecular mimicry [1]. Leukemia virus type I (HTLV-I) after a long incubation period. TSP/HAM is characterized by chronic progressive paraparesis with sphincter disturbances, no or mild sensory loss, absence of spinal cord compression, and seropositivity for HTLV-I antibodies. The pathogenesis of this entity, reviewed by Casseb and Penalva-de-Oliveira [6], is not completely clear and involves a multivariable phenomenon of activation of the immunological system against the presence of HTLV-I antigens, leading to an inflammatory process with axomyelinic degeneration, mainly in the thoracic spinal cord [7]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.