title: Initiation of HAART in drug-naive HIV type 1 patients prevents viral breakthrough for a median period of 35.5 months in 60% of the patients.
abstract: The introduction of potent combinations of antiviral drugs is a major breakthrough in the treatment of HIV. We investigated the long-term virologic outcome and the development of resistance after initiating highly active antiretroviral therapy (HAART) in drug-naive patients in daily clinical practice. Twenty-five treatment-naive HIV-1 patients were started on HAART. Fifteen patients responded with a drop in viral load below the limit of detection during 35.5 (interquartile range: 7) months of therapy. In 6 of 10 patients with virologic failure, virus with resistance-related mutations against the received drugs emerged. Compared with responders (R), nonresponding (NR) patients were in a later disease stage at therapy start (p = 0.0089) with lower CD4 cell counts at baseline (p = 0.040), and a lower proportion of nonresponders showed protease inhibitor (PI) levels above C(min) (p = 0.049). More NR patients showed secondary PI mutations at baseline (p = 0.079), and the CCR2-64I coreceptor polymorphism was absent among NR patients, compared with 38.5% of R patients displaying CCR2-64I (p = 0.053), although the differences were not significant. In conclusion, starting HAART in antiretroviral drug-naive HIV-infected patients followed in daily clinical practice prevented viral breakthrough for up to 44 months in 60% of the patients. Virologic failure was associated with the development of resistance-related mutations, a later stage of disease at start of therapy and lower PI drug levels.
authors.affiliation: Rega Institute for Medical Research and University Hospitals, Katholieke Universiteit Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium.
authors.forename: K
authors.initials: K
authors.lastname: Van Vaerenbergh
authors.forename: T
authors.initials: T
authors.lastname: Harrer
authors.forename: J-C
authors.initials: JC
authors.lastname: Schmit
authors.forename: A
authors.initials: A
authors.lastname: Carbonez
authors.forename: E
authors.initials: E
authors.lastname: Fontaine
authors.forename: M
authors.initials: M
authors.lastname: Kurowski
authors.forename: M
authors.initials: M
authors.lastname: Grünke
authors.forename: P
authors.initials: P
authors.lastname: Löw
authors.forename: A
authors.initials: A
authors.lastname: Rascu
authors.forename: B
authors.initials: B
authors.lastname: Schmidt
authors.forename: M
authors.initials: M
authors.lastname: Schmitt
authors.forename: I
authors.initials: I
authors.lastname: Thoelen
authors.forename: H
authors.initials: H
authors.lastname: Walter
authors.forename: K
authors.initials: K
authors.lastname: Van Laethem
authors.forename: M
authors.initials: M
authors.lastname: Van Ranst
authors.forename: J
authors.initials: J
authors.lastname: Desmyter
authors.forename: E
authors.initials: E
authors.lastname: De Clercq
authors.forename: A-M
authors.initials: AM
authors.lastname: Vandamme
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D005260:Female; D005838:Genotype; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1; D006801:Humans; D008297:Male; D009154:Mutation; D011110:Polymorphism, Genetic; D054390:Receptors, CCR2; D019713:Receptors, CCR5 / Q000235:genetics; D019707:Receptors, Chemokine / Q000235:genetics; D013997:Time Factors
chemical_list: C515334:CCR2 protein, human; D054390:Receptors, CCR2; D019713:Receptors, CCR5; D019707:Receptors, Chemokine; D054303:HIV Reverse Transcriptase; D016333:HIV Protease