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Prevalence of HIV-1 Syncytium-inducing Phenotype
- Michael J. Kozal, MD;
- Rani V. Ramachandran, MD; and
- Robert W. Shafer, MD
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TO THE EDITOR:
Koot and colleagues [1] reported that patients infected with human immunodeficiency virus (HIV) type 1 syncytium-inducing phenotype strains were more likely to progress to the acquired immunodeficiency syndrome (AIDS) than were patients with non-syncytium-inducing strains. Also, emergence of syncytium-inducing variants was associated with an accelerated CD4 cell decline, but it was not clear whether the relation was causal.
We agreed that it was important to know the prevalence of the syncytium-inducing phenotype, especially in patients enrolled in clinical trials, to guard against potential confounding by biased allocation of syncytium- and non-syncytium-inducing phenotypes. Consequently, we did a cross-sectional analysis of HIV-infected patients at Stanford's Center for AIDS Research to determine the prevalence of the syncytium-inducing phenotype in our West Coast referral population and its correlation with CD4+ T-cell levels. Using an MT-2 cell assay, we tested viral isolates from 197 patients enrolled in study protocols at Stanford [2]. The stage of disease varied from asymptomatic HIV infection to AIDS. The percentages of patients with the syncytium-inducing phenotype at various CD4 cell counts are shown in Table 1. Overall, 31% of patients harbored syncytium-inducing strains, and the prevalence of these strains was higher in the lower CD4 cell strata. These results concur with Koot and colleagues' finding that syncytium-inducing variants seem to emerge in patients with a CD4 count lower than 500 cells/µL. This finding is important because most clinical trials evaluating drug efficacy involve patients in this CD4 cell range. Most of our patients had significant declines in their CD4 cell counts in association with only the non-syncytium-inducing phenotype; this finding suggests that although a syncytium-inducing phenotype may be a cofactor in an accelerated decline in CD4 cells, it is not a prerequisite for significant immunologic deterioration in most patients.
Michael J. Kozal, MD
Rani V. Ramachandran, MD
Robert W. Shafer, MD
Stanford University Medical Center; Stanford, CA 94305
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
