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Departments of Psychiatry (Drs. Yoshioka, Shapshak, and Srivastava, and R. Stewart), Neurology (Drs. Shapshak, Bradley, and Berger), and Pathology (Drs. Shapshak and Nelson), University of Miami School of Medicine, Miami, FL; the Department of Neurology (Drs. Yoshioka and Nakamura), Tohoku University School of Medicine, Sendai, Miyagi, and the Neurology Service (Dr. Yoshioka), National Iwate Hospital, Ichinoseki, Iwate, Japan; the Departments of Pathology and Neurology (Dr. Rhodes), MetroHealth Medical Center and Case Western Reserve University, Cleveland, O H and the Department of Pathology (Dr. Sun), Harbor-UCLA Medical Center, Torrance, and Jonsson Comprehensive Cancer Center (Dr. Sun), Los Angeles, CA.
We examined the immunopathology and the expression of human immunodeficiency virus type 1 (HIV-1) in lumbosacral dorsal root ganglia (DRGs) from 16 patients with acquired immunodeficiency syndrome (AIDS) and 10 HIV-1-seronegative controls. Using in situ hybridization, we detected HIV-1 RNA in a few perivascular cells in DRGs from five of 16 AIDS patients (31%). In addition, using polymerase chain reaction, we detected HIV-1 DNA more frequently in DRGs from four of five AIDS patients (80%) examined. We detected interleukin-6 (IL-6) immunoreactivity in endothelial cells in DRGs from seven of 16 AIDS patients (44%) but from none of 10 HIV-1-seronegative controls (0%). We found more nodules of Nageotte, CD8+ T lymphocytes, and intercellular adhesion molecule-1 (ICAM-1)-positive endothelial cells and mononuclear cells in DRGs from AIDS patients than in DRGs from controls. Increased numbers of nodules of Nageotte in DRGs of AIDS patients were associated with detection of HIV-1 RNA by in situ hybridization and detection of IL-6 by immunohistochemistry. We conclude that low levels of replication of HIV-1, through cytotoxic T lymphocytes or expression of cytokines, may play a role in the subclinical degeneration of sensory neurons frequently observed in DRGs of AIDS patients.
Address correspondence and reprint requests to Dr. Masaru Yoshioka, Department of Neurology, Institute of Brain Diseases, Tohoku University School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai, Miyagi 980, Japan.
Supported in part by NIDA grants DA 04787 and DA 07909, NINDS grants NS 26584 and NS 31488, and Grant-in-AID for Scientific Research (C-05670544) of the Ministry of Education, Science, and Culture of Japan.
Received November 30,1992. Accepted for publication in final form December 13, 1993
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