Long-Term Seropositivity for Human T-Lymphotropic Virus Type III in Homosexual Men Without the Acquired Immunodeficiency Syndrome: Development of Immunologic and Clinical Abnormalities

A Longitudinal Study

  1. MADS MELBYE, M. D.;
  2. ROBERT J. BIGGAR, M.D.;
  3. PETER EBBESEN, M.D.;
  4. CAROLYN NEULAND, Ph.D.;
  5. JAMES J. GOEDERT, M.D.;
  6. VIGGO FABER, M.D.;
  7. IB LORENZEN, M.D.;
  8. PETER SKINHØJ, M.D.;
  9. ROBERT C. GALLO, M.D.; and
  10. WILLIAM A. BLATTNER, M.D.
  1. Aarhus, Copenhagen, and Hvidovre, Denmark; and Bethesda, Maryland

    Abstract

    The long-term effects of seropositivity for human T-lymphotropic virus type III (HTLV-III) on T-lymphocyte subsets and health status were evaluated in longitudinal studies of 250 initially healthy homosexual men. The relative risk of having an inverted T-lymphocyte helper-to-suppressor ratio rose from 14.3-fold among short-term seropositive subjects (less than 19 months) to 46.9-fold among long-term seropositive subjects (greater than 29 months) in comparison with the risk among seronegative subjects. Overall, 91.7% of long-term seropositive men had inverted ratios, compared with 12.9% of seronegative men. None of the seropositive men who developed an inverted ratio later reestablished a normal ratio. Both decreased T-helper cell number and percentage (p = 0.003) and increased T-suppressor cell number and percentage (p = 0.03) were significantly correlated with duration of seropositivity. Among seropositive persons, lymphadenopathy was a highly significant short-term as well as long-term consequence, whereas diarrhea, oral thrush, and herpes zoster were correlated with long-term seropositivity. Overall, 50% of long-term seropositive men compared with 16% of seronegative men developed at least one of five clinical symptoms (p < 0.003). We conclude that a high proportion of persons infected with HTLV-III will develop measurable immunologic and clinical abnormalities.

    Article and Author Information

    • ▸From the Institute of Cancer Research, Radiumstationen, Aarhus, the Department of Infectious Diseases and Department of Medicine, Rigshospitalet, Copenhagen, and the Department of Immunology and Rheumatic Diseases, Hvidovre Hospital, Hvidovre, Denmark; and the Environmental Epidemiology Branch, National Cancer Institute, the Department of Pathology, Uniformed Services University of Health Sciences, and the Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, Maryland.

    • Grant support: in part by grant 84-003 from the Danish Cancer Society and grant 12-5578 from the Danish Medical Research Council.

    • ▸Requests for reprints should be addressed to Mads Melbye, M.D.; Environmental Epidemiology Branch, National Cancer Institute, Landow Building 3C19; Bethesda, MD 20892.

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