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Ann Neurol. 1991 May;29(5):474-81.

Immunocytochemical and virological characteristics of HIV-associated inflammatory myopathies: similarities with seronegative polymyositis.

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Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.


We performed an immunoperoxidase study on muscle biopsy specimens from 19 patients with polymyositis who were seropositive for human immunodeficiency virus (HIV) (21 specimens) and 5 HIV-seronegative patients with polymyositis and compared the findings. A quantitative analysis of T cells and T-cell subsets, B cells, natural killer cells, interleukin-2 receptor-positive cells, and macrophages was performed on serial sections from all the specimens. Localization of major histocompatibility complex (MHC)-I and -II antigens, alpha and gamma interferon, and HIV antigens (p24, gp120, and gp41) was performed using specific antisera. In specimens from HIV-positive and seronegative patients, the predominant cell population was CD8+ cells and macrophages invading or surrounding healthy muscle fibers that expressed MHC-I antigen on their surface. The endomysial infiltrates in specimens from HIV-positive patients differed from those seen in specimens from the seronegative patients only by a significant reduction of the CD4+ cells (12.6 +/- 3.2% versus 21.1 +/- 4.2%). HIV antigens were seen in occasional interstitial mononuclear cells (but not in muscle fibers) in 6 of the 21 specimens from HIV-positive patients. Interferon was not localized. We conclude that the development of HIV-associated polymyositis does not appear to be related to direct infection of the muscle fibers by HIV but rather is due to a T-cell-mediated and MHC-I-restricted cytotoxic process, perhaps triggered by HIV. Because this immunopathological mechanism is common in both HIV-associated polymyositis and polymyositis alone, it is suggested that viruses may also be responsible in triggering polymyositis.

[Indexed for MEDLINE]

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