Do viral load and CD8 cell count at initiation of tritherapy influence the increase of CD4 T-cell count?
- 1 October 1998
- journal article
- Published by Wolters Kluwer Health in AIDS
- Vol. 12 (15) , F175-F179
- https://doi.org/10.1097/00002030-199815000-00002
Abstract
Tritherapies including protease inhibitors improve clinical status and usually increase CD4 T cell count. However, the dissociation between the marked decreases in viral load and the incomplete restoration of CD4 cell counts with a three-drug combination has been reported. We assessed this potential difference among our patients. Patients were enrolled when a protease inhibitor was prescribed to them for the first time. Using a computerized medical record (ADDIS), we retrospectively assessed a potential relationship between the increase in CD4 T cells (deltaCD4) at M3, M6 and variables including sex, age, CDC staging, protease inhibitor, prior antiviral therapy, CD8 and viral load at baseline. We used Epi-Info 6.4 and BMDP software. Data were analyzed on 154 patients. The median CD4 T cell count was 157 at baseline, 215 at month 3 and 202 at month 6. The median viral load was 52000 copies at baseline, 530 at month 3 and 500 at month 6. In a univariate analysis, a significant relationship was found between deltaCD4 and CD8 at baseline. A statistically significant negative correlation appeared between the CD8 cell count at baseline and deltaCD4 at M6 (r=-0.28, Pearson). Moreover, we found that there also was a relationship between deltaCD4 and viral load at baseline. There was a correlation between deltaCD4 at M6 and the viral load at M0 (r=0.37, Pearson). In a multiple regression model, after CD8 count at baseline had been accounted for, we found a significant correlation between deltaCD4 and viral load at baseline (multiple r=0.33 at M3, and 0.40 at M6). Patients with a low viral load do not benefit from as great an increase in CD4 T cell count as others when they receive a tritherapy including protease inhibitors. These results suggest that another mechanism rather than direct viral pathogenicity leads to CD4 T cell destruction. This mechanism may not be efficiently stopped by antiviral therapy, especially protease inhibitors.Keywords
This publication has 14 references indexed in Scilit:
- Treatment with Indinavir, Zidovudine, and Lamivudine in Adults with Human Immunodeficiency Virus Infection and Prior Antiretroviral TherapyNew England Journal of Medicine, 1997
- A Controlled Trial of Two Nucleoside Analogues plus Indinavir in Persons with Human Immunodeficiency Virus Infection and CD4 Cell Counts of 200 per Cubic Millimeter or LessNew England Journal of Medicine, 1997
- Preliminary Evidence for Partial Restoration of Immune Function in HIV Type 1 Infection with Potent Antiretroviral Therapies: Clues from the Fourth Conference on Retroviruses and Opportunistic DiseasesAIDS Research and Human Retroviruses, 1997
- Plasma Viral Load and CD4+ Lymphocytes as Prognostic Markers of HIV-1 InfectionAnnals of Internal Medicine, 1997
- Monitoring Plasma HIV-1 RNA Levels in Addition to CD4+ Lymphocyte Count Improves Assessment of Antiretroviral Therapeutic ResponseAnnals of Internal Medicine, 1997
- Prognosis in HIV-1 Infection Predicted by the Quantity of Virus in PlasmaScience, 1996
- Immunopathogenic Mechanisms of HIV InfectionAnnals of Internal Medicine, 1996
- Glucocorticoids rescue CD4+ T lymphocytes from activation-induced apoptosis triggered by HIV-1AIDS, 1995
- Multifactorial Nature of Human Immunodeficiency Virus Disease: Implications for TherapyScience, 1993
- Safety and Efficacy of Polyethylene Glycol-Modified Interleukin-2 and Zidovudine in Human Immunodeficiency Virus Type 1 Infection: A Phase I/II StudyThe Journal of Infectious Diseases, 1993