Explaining, Predicting, and Treating HIV-Associated CD4 Cell Loss
After 25 Years Still a Puzzle
- W. Keith Henry, MD;
- Pablo Tebas, MD;
- H. Clifford Lane, MD
- Author Affiliations: HIV Program, Hennepin County Medical Center and the University of Minnesota, Minneapolis (Dr Henry); Division of Infectious Diseases, University of Pennsylvania, Philadelphia (Dr Tebas); and Division of Clinical Research and Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Md (Dr Lane).
- Corresponding Author: Keith Henry, MD, Hennepin County Medical Center, 701 Park Ave R7, Minneapolis, MN 55415 (keithh6680{at}aol.com).
Since this article does not have an abstract, we have provided the first 150 words of the full text.
- KEYWORDS:
- COLORECTAL NEOPLASMS, HEREDITARY NONPOLYPOSIS
- GENETIC PREDISPOSITION TO DISEASE
- GENETIC SCREENING
- MUTATION
- PROGNOSIS
- SEQUENCE ANALYSIS, DNA
The clinical syndrome of AIDS is due to infection with the human immunodeficiency virus (HIV), which causes a progressive immunodeficiency characterized by the loss of CD4 T lymphocytes coupled with an immunosuppression related to global activation of the immune system. Since the seminal article by Mellors et al in 1996,1 it has been known that as a group, individuals with a higher HIV RNA viral load tend to progress to AIDS and death at a more rapid rate than those with lower viral loads, and that different prognostic information can be derived from the CD4 cell count and the viral load. The conventional wisdom is that the CD4 cell count represents the current state of immune deficiency, whereas the viral load reflects the rate at which the immune system will further deteriorate.2
The report by Rodríguez and colleagues3 in this issue of JAMA challenges the notion that, …
