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Impact on Markers of HIV Disease Progression

Mauro Schechter, MD, PhD; Lee H. Harrison, MD; Neal A. Halsey, MD; Georgia Trade, MD; Marcelo Santino; Lawrence H. Moulton, PhD; Thomas C. Quinn, MD

JAMA. 1994;271(5):353-357.

Abstract
Objectives.
—To study the effect of human T-cell lymphtropic virus type I (HTLV-I) on markers of human immunodeficiency virus (HIV) disease progression.

Design.
—A retrospective, nested case-control study.

Setting.
—A university hospital outpatient HIV clinic in Rio de Janeiro, Brazil.

Participants.
—Human immunodeficiency virus—seropositive adults participating in a prospective HIV cohort study.

Main Outcome Measures.
—The HIV clinical stage, CD4⁺ lymphocyte counts, and other laboratory parameters in 27 individuals infected with HIV and HTLV-I (coinfection) and 99 age-matched, HIV-seropositive, HTLV-seronegative controls (single infection).

Results.
—Variables independently associated with coinfection included higher CD4⁺ lymphocyte count (odds ratio [OR], 2.3; 95% confidence limits [CL], 1.3,4.1), higher CD4⁺ percentage (OR, 2.0; 95% CL, 1.3, 3.2), β₂-microglobulin level of 254 nmol/L or more (OR, 6.8; 95% CL, 1.3, 35.4), World Health Organization stages 3 and 4 (OR, 4.4; 95% CL, 1.1,18.0), and reporting a parenteral risk factor (OR, 7.4; 95% CL, 1.4, 38.9). When stratified by p24 antigenemia, coinfection was associated with an estimated 82% higher CD4⁺ lymphocyte count (P<.05).

Conclusion.
—Coinfection was associated with higher CD4⁺ lymphocyte counts, more advanced clinical disease, and higher β₂-microglobulin levels than HIV infection alone. The higher mean CD4⁺ lymphocyte count does not appear to offer immunologic benefit. Caution should be exercised when using CD4⁺ lymphocytes as a surrogate marker in studies of HIV infection in populations where HTLV-I is prevalent. Further studies are needed to address whether current CD4⁺ lymphocyte values for the initiation of antiretroviral therapy and chemoprophylaxis against opportunistic infections in HIV infection are appropriate in coinfection.

(JAMA. 1994;271:353-357)

Author Affiliations
From the Infectious Diseases Service, Department of Preventive Medicine, Hospital Universitário Clementino Fraga Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil (Drs Schechter and Trade and Mr Santino); the Departments of International Health (Drs Harrison, Halsey, and Moulton) and Biostatistics (Dr Moulton), School of Hygiene and Public Health, and the Departments of Medicine (Drs Harrison and Quinn), and Pediatrics (Dr Halsey), School of Medicine, Johns Hopkins University, Baltimore, Md; and the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md (Dr Quinn).

Footnotes
Reprint requests to the Department of International Health, School of Hygiene and Public Health, Johns Hopkins University, Room 5515, 615 N Wolfe St, Baltimore, MD 21205 (Dr Harrison).

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