Effect of Antiretroviral Therapy on Viral Load, CD4 Cell Count, and Progression to Acquired Immunodeficiency Syndrome in a Community Human Immunodeficiency Virus–Infected Cohort

Abstract

Objective: To examine the effect of different antiretroviral treatment regimens on viral load, CD4 lymphocyte counts, and rates of progression to clinical acquired immunodeficiency syndrome events among treatment-naive human immunodeficiency virus (HIV)-infected patients enrolled in a large community cohort study.Methods: Based in 7 outpatient clinics, the Swiss HIV Cohort Study is a cohort with national coverage. Virological, immunologic, and clinical results of 755 treatmentnaive patients (median age, 36 years; 28.2% female) who initiated antiretroviral therapy between July 1, 1995, and June 30, 1997, were analyzed. Patients started undergoing monotherapy with 1 reverse transcriptase inhibitor (RTI), combination therapy with at least 2 RTIs, or highly active antiretroviral therapy (HAART) with RTIs and protease inhibitors.Results: Antiretroviral treatment led to a mean reduction of viremia of 1.8 log 10 copies per milliliter with HAART, 1.2 log 10 copies per milliliter with RTI combination therapy, and 0.4 log 10 copies per milliliter with monotherapy. Virological failure, defined as less than 1 log 10 reduction per milliliter in viremia, was present in 45 (20%) patients undergoing HAART, 180 (38%) undergoing RTI combination therapy, and 47 (82%) undergoing monotherapy. The proportion of patients reaching undetectable viremia was 12% (n = 7) for monotherapy, 41% (n = 197) for RTI combination therapy, and 63% (n = 137) for HAART. Similar gains of CD4 cells were achieved with RTI combination therapy and HAART. Kaplan-Meier estimates of progression rates to a new acquired immunodeficiency syndrome event at 18 months were 13.6% (monotherapy), 4.7% (RTI combination therapy), and 3.9% (HAART). Conclusions:The rate of virological failure of antiretroviral treatments was high in this population of treatment-naive patients, even among patients receiving combination regimens. Clinical progression rates were, however, low in patients treated with RTI combination therapy and HAART.

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“…PI-based combination regimens can lead to profound and sustained suppression of viral replication (9,13,20); however, these regimens eventually fail to control replication in a significant portion of patients, leading to the eventual development of resistant viruses (10,14,18). Although failure of PIbased therapy has a complex and multifactorial etiology, inadequate drug concentrations in plasma due to poor or variable pharmacokinetics and/or inconsistent adherence appear to be important factors (1,7,16,19,26,38,42).…”

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“…17 This difference might be explained by the general improvement of education in all the sectors in developing countries. 18 …”