Effects on immunological and virological outcome of patients using one protease inhibitor or one non-nucleoside reverse transcriptase inhibitor in a triple antiretroviral therapy: normal clinical practice versus clinical trial findings.
We compared the response of two standard 3-drug regimens containing two-nucleoside reverse transcriptase inhibitor (Zidovudine +Lamivudine) plus either a protease inhibitor (PIs) (Indinavir) or a non-nucleoside reverse transcriptase inhibitor (NNRTIs) (Efavirenz) among treatment-naïve or treatment-experienced HIV-infected persons. The obtained results will be compared to clinical trial findings. Through a retrospective study, we compared the virological and immunological response of 119 Tunisian HIV-1 infected patients (North Africa) who started for the first time/ in salvage use a triple antiretroviral treatment containing one NNRTI (group A1/group A2) or one PI (group B1/group B2). Viral load (VL) was analysed with Amplicor HIV-1 Monitor test and drug resistance mutations were examined by using two distinct line probe assays (LiPA). The analysis according to the received treatment showed an average of 0.45 log(10) drop in the mean VL among groups A2 and B2. For naïve patients, 62.5% of group A1 reached an undetectable VL versus 53.5% for group B1 (p < 0.001). With regard to the CD4 cell count change, we observed a mean increase of more than 65% versus baseline within group A1 in comparison with 42% for group B1 (p < 0.001). Genotypic resistance assays showed that patients of group A2 had significantly more resistance mutations than those of group B2 (2.66 vs. 0.75 (p = 0.0039)). Finally, 15 patients who were failing were switched to indinavir or efavirenz. When indinavir was replaced by efavirenz, we observed an increase in the plasma VL. With regard to the effects on immunological and virological outcome of patients using PIs or NNRTIs in a triple antiretroviral therapy, our observations in normal clinical practice supported the reported clinical trial findings but are not in favour of replacing indinavir by efavirenz in failing regimen.
Fethi
Tebourski
T
Laboratoire de Génétique Moleculaire, Immunologie, et Biotechnologie, Faculté des Sciences de Tunis, Université Tunis, Tunisia. fateb@planet.tn
Asma
Jlizi
J
Amine
Slim Mohamed
SM
Amel
Elgaaied-Ben Ammar
EB
Taoufik
Ben Chaabane
BC
Mohamed
Chakroun
C
Amel
Letaief-Omezzine
LO
Mounira
Garbouj
G
D000328:Adult; D000480:Alkynes; D023241:Antiretroviral Therapy, Highly Active; D048588:Benzoxazines; D015331:Cohort Studies; D003521:Cyclopropanes; D024882:Drug Resistance, Viral / Q000235:genetics; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D019469:Indinavir / Q000008:administration & dosage; D019259:Lamivudine / Q000008:administration & dosage; D008297:Male; D010078:Oxazines / Q000008:administration & dosage; D012189:Retrospective Studies; D016896:Treatment Outcome; D014416:Tunisia; D014766:Viremia / Q000188:drug therapy / Q000276:immunology / Q000821:virology; D015215:Zidovudine / Q000008:administration & dosage
D000480:Alkynes; D048588:Benzoxazines; D003521:Cyclopropanes; D010078:Oxazines; D019259:Lamivudine; D015215:Zidovudine; D019469:Indinavir; C098320:efavirenz