Identification of human t cell leukemia/lymphoma virus type i antibodies, dna, and protein in patients with polymyositis

• Published in: Arthritis and rheumatism 1995-05, Vol.38 (5), p.690-698
• Main Authors: Sherman, Michael P., Amin, Rajnikant M., Rodgers‐Johnson, Pamela E. B., Morgan, Owen S. C., Char, Gurendra, Mora, Carlos A., Iannone, Robert, Collins, George H., Papsidero, Lawrence, Gibbs, Clarence J., Poiesz, Bernard J.
• Format: Article
• Language: English
• Subjects: Adult; AIDS/HIV; Base Sequence; Biological and medical sciences; Biopsy; DNA, Viral - isolation & purification; Female; Gene Products, env - analysis; HTLV-I Antibodies - blood; Humans; Male; Medical sciences; Middle Aged; Molecular Sequence Data; Muscles - chemistry; Muscles - pathology; Polymerase Chain Reaction; Polymyositis - blood; Polymyositis - immunology; Polymyositis - pathology; Polymyositis - virology; Retroviridae Proteins, Oncogenic - analysis; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
• ISSN: 0004-3591; 1529-0131
• DOI: 10.1002/art.1780380518

Objective. To investigate a possible association between human T cell leukemia/lymphoma virus type I (HTLV‐I) and polymyositis (PM). Methods. Sera and muscle biopsy samples from 9 Jamaican PM patients were compared with specimens from American HTLV‐I–positive PM patients and normal controls. Sera were evaluated for HTLV antibodies by enzyme‐linked immunosorbent assay and Western blot. The biopsy samples were analyzed for HTLV‐I/II DNA by polymerase chain reaction and were also immunohistochemically stained for HTLV gp46 envelope protein. Results. Seven of the 8 Jamaican PM patients from whom sera were available were HTLV‐I seropositive. The muscle biopsies of all 9 Jamaican patients demonstrated severe lymphocytic infiltration, cellular degeneration, myofiber atrophy, and fibrosis. Each muscle biopsy specimen contained HTLV‐I DNA. Two of 6 samples demonstrated intense staining for HTLV‐I gp46 in many of the invading mononuclear cells and weak staining for HTLV‐I gp46 in many of the invading mononuclear cells and weak staining in the adjacent myocytes. Two other specimens were weakly positive for gp46 in rare mononuclear cells. All control specimens were negative for the presence of HTLV‐I DNA and protein. Conclusion. HTLV‐I is associated with an inflammatory muscle disease characterized by direct invasion of the affected muscle by HTLV‐I–infected mononuclear cells.