Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

Our group has previously reported that a significantly larger proportion of peripheral monocytes from human immunodeficiency virus type 1 (HIV-1) seropositive individuals receiving highly active antiretroviral therapy (HAART) express HLA-G1 [1] and also that one of the HAART components, the nucleoside reverse transcriptase inhibitors (NRTIs), may be involved in this effect [2]. Because protease inhibitors (PIs) are another component of HAART that are administered with NRTIs, the aim of this work was to determine whether or not PIs are also involved in the HLA-G1 changes previously observed in treated HIV-1 positive patients. CD14+ cells expressing HLA-G1 were therefore measured in 7 HIV-1 positive patients whose initial HAART was changed to a protease inhibitor–only regime due to drug toxicity and/or virologic resistance. Our results indicate that PIs do not appear to be implicated in the rise of HLA-G1 expression on CD14+ cells from HIV-1 infected individuals receiving HAART, while we further confirm that NRTIs are involved in the surface induction of HLA-G1.