Arthritis in patients infected with human T lymphotropic virus type I. Clinical and immunopathologic features

Abstract

Ten patients with chronic inflammatory arthropathy and the human T lymphotropic virus type I (HTLV-I) are described. These patients showed chronic persistent oligoarthritis, associated with proliferative synovitis, in large joints. The place of birth or residence of these patients was within the area endemic for adult T cell leukemia (ATL) and HTLV-I. The age at onset of articular symptoms tended to be higher in these patients than in typical rheumatoid arthritis patients. Anti-HTLV-I antibodies were detected in both sera and synovial fluids from all patients. Western blot analysis revealed antibodies to viral gag proteins (p19, p24, and p28). Atypical lymphocytes with nuclear indentations, consistent with ATL-like cells, were observed in both synovial fluid and synovial tissue. Furthermore, HTLV-I proviral DNA was integrated into the DNA of

Molecular and cellular aspects of HTLV-1 associated leukemogenesis in vivo

“…2,3 Furthermore, this virus has been associated with the development of a chronic progressive neuromyelopathy (tropical spastic paraparesis (TSP)/HTLV-1-associated myelopathy (HAM)), 4 and, to a lesser extent, to a variety of inflammatory diseases. [5][6][7][8][9] Among the 15-25 million individuals infected worldwide, approximately 3% to 5% will develop ATLL, depending on as yet unknown cofactors. ATLL harbors different clinical features resulting in a division of the spectrum of the disease into four clinical subtypes 10,11 referred to as acute, lymphoma, chronic and smoldering subtypes.…”

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

“…Furthermore, this virus has been associated, though to a lesser extent, to the development of a variety of in¯ammatory diseases (Eguchi et al, 1992;LaGrenade et al, 1990;Mattos et al, 1993;Mochizuki et al, 1994;Sato et al, 1991;Sherman et al, 1995). Among the 15 ± 25 million individuals infected worldwide, approximately 3 ± 5% will develop ATLL, depending on as yet unknown cofactors.…”

Development of Graves' Ophthalmopathy and Uveitis after Radioiodine Therapy for Graves' Disease in a Patient with HTLV-I Associated Myelopathy (HAM).

“…The mechanism by which spinal cord degeneration is caused by HTLV-I infection is considered to be immunologic (8,9). The association of Graves' disease with HAM is not incidental, because the incidence of manyother autoimmunediseases or immune-mediated diseases are high in HAM patients or HTLV-I carriers (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23).…”