title: Improved long-term suppression of HIV-1 replication with a triple-class multidrug regimen compared with standard of care antiretroviral therapy.
abstract: BACKGROUND
  The treatment of HIV-1-infected patients with triple-drug combination therapy results in profound suppression of viral replication. In most therapy-naive patients plasma HIV-1-RNA levels (pVL) drop below the lower limit of quantification (LLQ) of currently used assays. In a large percentage of such patients, more sensitive assays provide evidence of residual viral replication. The question is whether more potent therapy can further suppress this residual replication.
  
  
  METHODS
  Thirty control patients who, using very strict criteria, had not experienced virological failure during 3 years of standard therapy, were compared with 10 patients treated with a five-drug regimen, consisting of three different classes of antiretroviral drugs (alternative multidrug regimen). A modified ultrasensitive assay with an LLQ of 5 copies/ml was used to re-test plasma obtained at week 48 and at three timepoints at and around week 144.
  
  
  RESULTS
  At weeks 48 and 144 pVL could be quantified significantly more frequently in control patients than in patients using the alternative multidrug regimen (week 48: 42 versus 0% with quantifiable pVL, P = 0.017; week 144: 60 versus 14% with at least one quantifiable pVL, P = 0.036, respectively). A low baseline CD4T cell count was predictive of quantifiable pVL in control patients, but not in alternative multidrug patients.
  
  
  CONCLUSIONS
  This proof-of-principle study demonstrates that the use of an alternative multidrug regimen results in stronger long-term suppression of pVL compared with clinically successful treatment with standard therapy.
authors.affiliation: National AIDS Therapy Evaluation Center (NATEC), Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, University of Amsterdam, The Netherlands.
authors.forename: Rieneke M E
authors.initials: RM
authors.lastname: van Praag
authors.forename: Ferdinand W N M
authors.initials: FW
authors.lastname: Wit
authors.forename: Suzanne
authors.initials: S
authors.lastname: Jurriaans
authors.forename: Frank
authors.initials: F
authors.lastname: de Wolf
authors.forename: Jan M
authors.initials: JM
authors.lastname: Prins
authors.forename: Joep M A
authors.initials: JM
authors.lastname: Lange
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D015224:Dideoxynucleosides / Q000627:therapeutic use; D005500:Follow-Up Studies; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology; D015497:HIV-1 / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D019469:Indinavir / Q000627:therapeutic use; D019259:Lamivudine / Q000627:therapeutic use; D008875:Middle Aged; D019829:Nevirapine / Q000627:therapeutic use; D012367:RNA, Viral / Q000187:drug effects; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use*; D013997:Time Factors; D019562:Viral Load; D014779:Virus Replication / Q000187:drug effects*; D015215:Zidovudine / Q000627:therapeutic use; D000099227:Abacavir
chemical_list: D019380:Anti-HIV Agents; D015224:Dideoxynucleosides; D019469:Indinavir; D019259:Lamivudine; D019829:Nevirapine; D012367:RNA, Viral; D018894:Reverse Transcriptase Inhibitors; D015215:Zidovudine; D000099227:Abacavir