FOSCARNET DECREASES HIV-1 PLASMA LOAD

Objective: To evaluate the effect of foscarnet on HIV-1 replication in vivo. Patients and Methods: Seventeen AIDS patients with cytomegalovi rus (CMV), herpes simplex virus (HSV), varicella-zoster virus (VZV) in fection, Kaposi's sarcoma (KS), or a combination of these were treated with foscarnet. HIV RNA quantification (bDNA 2.0, Chiron, Emeryville, CA, U.S.A.), CMV pp65 antigenemia (Argene Biosoft, Varilhes, France), and CMV viremia were determined before and during therapy. Results: F our patients had CMV retinitis (1 with KS), 2 patients had CMV pneumon ia (1 with KS), 1 patient had CMV cholecystitis, 2 patients had VZV in fection (1 with KS), 1 patient had HSV-2 infection, and 7 patients had KS alone. The decrease in HIV-1 load was -0.73 +/- 0.39 log copies/ml (p = 2.10(-6)) sifter 3 days of treatment and -1.15 +/- 0.49 log copi es/ml (p < 10(-7)) after 10 days of treatment, compared with day 0. Fu rthermore, reduction of HIV-1 plasma load during foscarnet therapy did not depend on the presence or absence of CMV disease or on a positive pp65 antigenemia at day 0. Conclusion: We observed decreased HIV-1 pl asma load in all patients treated with foscarnet, regardless of presen ce or absence of clinical or biologic CMV infection. This decrease sup ports the proposition that foscarnet anti-HIV-1 activity may be of cli nical importance.