Guest guest Posted September 26, 2006 Report Share Posted September 26, 2006 [Moderators note: Abstract of the original article and the summary of this week's Journal of the American Medical Association. (JAMA) follows the news item] HIV 'Viral load' not indicative of AIDS progress - study Wed Sep 27, 2006 1:45 AM IST CHICAGO (Reuters) - Measuring the amount of AIDS virus circulating in the blood of HIV-positive patients is not a good indicator of the health of their immune systems, researchers said on Tuesday. Physicians often assess the amount of HIV particles in the blood -- known as the viral load -- along with the decline in CD4 cells that help the body fight infections to measure the disease's progress and decide when to prescribe drug therapy. But a study of 2,800 untreated HIV-positive individuals found only about 5 percent of the variations in viral load corresponded to variations in immune system damage. Depletion of CD4 cells is therefore not a simple consequence of the amount of virus circulating, said the study published in this week's Journal of the American Medical Association. " The results of this nationwide study may have profound implications in our understanding of how HIV causes disease and in our approach to the management of HIV-infected patients, " said lead investigator Dr. Benigno of Case Western Reserve University in Cleveland. Estimating damage to the immune system is critical in deciding when it is best to start antiretroviral therapy, the AIDS-fighting drugs credited with allowing millions of infected people to live with the disease. Because of issues of drug resistance and the potent side effects of the drugs, doctors and patients often defer starting medications until medically necessary. The study challenges the current belief that the degree to which the virus replicates itself is the trigger for the loss of CD4 cells, white blood cells that are a key component of the body's immune system. An accompanying editorial in the journal said the findings were exciting because they suggested that researchers should look for and target non-viral factors that set off the eventual decline in the immune system. http://in.today.reuters.com/news/newsArticle.aspx? type=worldNews & storyID=2006-09-27T013224Z_01_NOOTR_RTRJONC_0_India- 269451-1.xml & archived=False ___________________________ Editorial Explaining, Predicting, and Treating HIV-Associated CD4 Cell Loss: After 25 Years Still a Puzzle W. Henry, MD; Pablo Tebas, MD; H. Clifford Lane, MD JAMA. 2006;296:1523-1525. (This article does not have an abstract, the first 150 words of the full text is provided) 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 ________________________ Predictive Value of Plasma HIV RNA Level on Rate of CD4 T-Cell Decline in Untreated HIV Infection Benigno Rodríguez, Ajay K. Sethi, Vinay K. Cheruvu, Wilma Mackay, J. Bosch, Mari Kitahata, L. Boswell, W. Mathews, R. Bangsberg, , C. Whalen, Sieg, Suhrida Yadavalli, G. Deeks, and M. Lederman JAMA. 2006;296:1498-1506. Context: Plasma human immunodeficiency virus (HIV) RNA level predicts HIV disease progression, but the extent to which it explains the variability in rate of CD4 cell depletion is poorly characterized. Objective: To estimate the proportion of variability in rate of CD4 cell loss predicted by presenting plasma HIV RNA levels in untreated HIV-infected persons. Design: Repeated-measures analyses of 2 multicenter cohorts, comprising observations beginning on May 12, 1984, and ending on August 26, 2004. Analyses were conducted between August 2004 and March 2006. Setting Two cohorts of HIV-infected persons: patients followed up at 4 US teaching medical institutions or participating in either the Research in Access to Care for the Homeless Cohort (REACH) or the San Francisco Men's Health Study (SFMHS) cohorts and participants in the Multicenter AIDS Cohort Study (MACS) cohort. Participants: Antiretroviral treatment–naive, chronically HIV- infected persons (n = 1289 and n = 1512 for each of the 2 cohorts) untreated during the observation period ( 6 months) and with at least 1 HIV RNA level and 2 CD4 cell counts available. Approximately 35% were nonwhite, and 35% had risk factors other than male-to-male sexual contact. Main Outcome Measures: The extent to which presenting plasma HIV RNA level could explain the rate of model-derived yearly CD4 cell loss, as estimated by the coefficient of determination (R2). Results In both cohorts, higher presenting HIV RNA levels were associated with greater subsequent CD4 cell decline. In the study cohort, median model–estimated CD4 cell decrease among participants with HIV RNA levels of 500 or less, 501 to 2000, 2001 to 10 000, 10 001 to 40 000, and more than 40 000 copies/mL were 20, 39, 48, 56, and 78 cells/µL, respectively. Despite this trend across broad categories of HIV RNA levels, only a small proportion of CD4 cell loss variability (4%-6%) could be explained by presenting plasma HIV RNA level. Analyses using multiple HIV RNA measurements or restricting to participants with high HIV RNA levels improved this correlation minimally (R2, 0.09), and measurement error was estimated to attenuate these associations only marginally (deattenuated R2 in the 2 cohorts, 0.05 and 0.08, respectively). Conclusions Presenting HIV RNA level predicts the rate of CD4 cell decline only minimally in untreated persons. Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection. These findings have implications for treatment decisions in HIV infection and for understanding the pathogenesis of progressive immune deficiency. Author Affiliations: Center for AIDS Research (Drs Rodríguez, Sieg, and Lederman, and Mrs Yadavalli), Center for Modern Epidemiology of Infectious Diseases (Drs Sethi and Whalen and Mr Cheruvu and Ms Mackay), Case Western Reserve University, Cleveland, Ohio; Department of Biostatistics, Harvard School of Public Health, Harvard University, Boston, Mass (Dr Bosch); Department of Medicine, University of Washington, Seattle (Dr Kitahata); Department of Medicine, Harvard University School of Medicine, Boston, Mass (Dr Boswell); Department of Medicine, University of California, San Diego (Dr Mathews); Department of Medicine and Epidemiology (Drs Bangsberg and ) and Department of Medicine (Dr Deeks), University of California, San Francisco. Quote Link to comment Share on other sites More sharing options...
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