Viral load and burden modification following early antiretroviral therapy of primary HIV-1 infection

Objective: The aim of this study was to monitor the effect on viral DNA and RNA of early treatment with highly aggressive antiretroviral therapy (HAAR T), in comparison with zidovudine (ZDV) monotherapy or no treatment in subj ects with primary HIV-1 infection (PHI). Design and methods: Of the 28 patients selected, four were untreated, four received ZDV alone, 10 received a triple combination (ZDV, lamivudine (3TC) and saquinavir (SQV)) and 10 received a quadruple combination (ZDV, 3TC, S QV and ritonavir (RTV)). Seroconversion was monitored by means of Western b lot profile analysis. A quantitative polymerase chain reaction (PCR) assay in the HIV gag region was used to monitor viral DNA and the nucleic acid se quence based amplification (NASBA) system for viraemia (HIV-RNA). Results: There was a certain level of heterogeneity in the baseline values of HIV-DNA and RNA. Early HAART led to a rapid recovery in the number of CD 4 cells and the CD4/CD8 cell ratio and a reduction in HIV-RNA to undetectab le levels, which was significantly greater than in the untreated patients o r those treated with ZDV. Although a reduction in DNA levels was also obser ved in the HAART-treated subjects, this variation was not significant. Conclusions: The parameters of viral replication and CD4 cell recovery were only slightly better in the patients receiving ZDV monotherapy than in the untreated patients, thus confirming that the course of the infection is ha rdly affected by the monotherapy. The early introduction of HAART greatly r educes plasma viraemia and restores the number of CD4 cells for up to 1 yea r. HIV-DNA remains detectable, although at low levels, thus confirming that the early established reservoir of infected cells is little affected. Long er periods of observation and the introduction of complementary approaches, such as immunomodulatory therapies, will provide further information conce rning the possibility of radically interfering with the natural evolution o f the disease. (C) 1999 Lippincott Williams & Wilkins.