NNRTI, PI or INSTI-based therapies, in combination with a dual-NRTI backbone,
provide effective suppression of HIV-1 replication and reconstitution of CD4 cell counts. A
randomized prospective trial of 1,400 subjects demonstrated similar composite endpoints of
death, AIDS-defining event or CD4 count decline to <200 cells/µL, in subjects receiving either
an NNRTI- or PI-based regimen (34). A meta-analysis of clinical trials comparing NNRTI- and
PI-based therapy suggested that NNRTI-based therapy was more effective than PI-based therapy
for virologic suppression, but was similar to PI-based therapy for clinical outcomes (7). The low
genetic barrier to resistance to NNRTIs, where single nucleotide substitutions may confer broad
class-wide resistance (except for etravirine), provides an additional rationale for the first use of a
boosted PI when adherence may be a problem. However, NNRTI-based regimens may have
lower pill burdens and provide greater convenience (particularly the fixed-dose regimen of
tenofovir/emtricitabine/efavirenz), and possibly improved lipid profiles, when compared to PIbased
regimens. Although there is less experience with INSTI-based regimens, studies to date
show similar virologic outcomes with raltegravir when compared to efavirenz, when either is
combined with tenofovir and emtricitabine, over 96 weeks of observation (37).
การแปล กรุณารอสักครู่..