TreatmentUpdate 76. 9(2): 4; March, 1997
Sean Hosein
Study details
For this study doctors at Ottawa General Hospital recruited 43 HIV-infected subjects who had never before used protease inhibitors. Fifty percent of subjects had a CD4+ count of 300 cells. They received a combination of ritonavir and saquinavir.
Results ? CD4+, viral load
By the 6th month of the study, the average CD4+ count rose to 400 cells and the average viral load fell to 1/10,000th of its pre-study level. These changes were statistically significant.
The immune system
The CD4+ cells of subjects seemed better able to respond to infections (in lab experiments). This is probably due to ritonavir?s anti-HIV activity. It is possible that the drug also stimulates the immune system. To find out more about how these drugs affect the immune system they should also be studied in healthy, non-HIV infected people. Unfortunately, this is difficult because such people refuse to take the drug for long periods because of its side effects. Although improvements in CD4+ function are encouraging, researchers aren?t sure that these will result in better control of infections outside of the lab, that is, in the bodies of PHAs.
T cells in Australia
Another research team in Australia also studied the effect of ritonavir on T cells. They found that after 1 month of ritonavir therapy, T cells (taken from subjects) were able to produce increased amounts of the chemicals IL-2 and interferon-gamma compared to T cells taken from subjects receiving fake ritonavir. These differences were statistically significant; that is, likely due to the effect of ritonavir and not luck. Although production of IL-2 and interferon-gamma increased, their levels were still less than normal. As well, CD8+ cells produced much more of these chemicals than did CD4+ cells.
REFERENCES:
1.Angel JB, Parato K, Kumar A, et al. Rapid improvement in cell-mediated immune function with initiation of ritonavir plus saquinavir in HIV immune deficiency. Oral presentation, abstract 33.
2. Gorochov G, Kereveur A, Parizot C, et al. TCR-b repertoire complexity and evolution of HIV infection: influence of anti-retroviral regimens including protease inhibitors. Abstract 110.
3. Valette M, Gerard Y, Ajana F, et al. Kaplan-Meir analysis of interruption probability of a protease inhibitor, saquinavir (S), indinavir (I) or ritonavir (R) in 177 patients receiving a combination of protease inhibitors and reverse transcriptase inhibitors (RTI). Abstract 197.
4. Autran B, Mathez D, Carcelain G, et al. Dynamics of the CD4+ T helper cell subset reconstitution after combined anti-retroviral therapies. Oral presentation, abstract 34.
5. Kelleher AD, Zaunders J, Sewell W, et al. Increased proliferative and cytokine responses following ritonavir therapy: relative contribution of lymphocyte subsets. Abstract 536.
970320
CATE7604
Copyright © 1997 - TreatmentUpdate. Reproduced with permission. Reproduction of this article (other than one copy for personal reference) must be cleared through the Editor, The Canadian AIDS Treatment Information Exchange, 555 Richmond St. West, Suite 505, Box 1104, Toronto, ON, M5V 3B1 • Phone: 416-203-7122 • Toll Free: 1-800-263-1638 • Fax: 416-203-8284 http://www.catie.ca
Disclaimer: The editors have taken all such care as they consider reasonable in preparing this database, but they cannot be held responsible for any inaccuracies or mis-statements of fact contained herein. Inclusion in this database of any information on any treatment, therapy, or clinical trial in no way represents an endorsement of that treatment, therapy, or trial by ÆGiS or any of its sponsors. This data should always be used in conjunction with professional medical advice.