title: Proviral HIV-1 DNA in subjects followed since primary HIV-1 infection who suppress plasma viral load after one year of highly active antiretroviral therapy.
abstract: OBJECTIVE
  An assessment of the impact of one year potent antiretroviral treatment initiated during primary HIV infection on the cell-associated viral burden.
  
  
  METHODS
  Proviral HIV-1 DNA was quantified in serial peripheral blood mononuclear cell (PBMC) samples from 19 patients enrolled in the French prospective PRIMO Cohort for whom plasma HIV RNA was suppressed to undetectable levels after one year of triple therapy; that is, plasma HIV-1 RNA was maintained below 200 copies/ml. Results were compared with those observed in 19 patients with chronic HIV-1 infection presenting the same degree of virus suppression after 12 months of treatment.
  
  
  RESULTS
  At study entry, PRIMO subjects presented heterogeneous levels of proviral HIV-1 DNA: 2-3.92 log10 copies/10(6) PBMC and plasma HIV RNA: 2.3-6.5 log10 copies/ml. One year of effective highly active antiretroviral therapy (HAART) resulted in a median diminution of proviral DNA of -0.78 log10/10(6) PBMC in PRIMO subjects. The median decline in chronic-phase patients was -0.32 for those who were pre-treated and -0.52 for those previously naive of treatment.
  
  
  CONCLUSIONS
  The decline in cell-associated HIV DNA observed throughout one year treatment indicated that HAART reduces the proviral HIV-DNA load more effectively when initiated during the primary rather than the chronic phase of HIV infection. These findings therefore tend to lend support to the early initiation of treatment. Nevertheless, heterogeneous baseline values observed for CD4 cell count, plasma HIV RNA and proviral HIV DNA in PRIMO subjects, raise the question of whether treatment should be delayed in some to spare early adverse effects of HAART.
authors.affiliation: Laboratoire de Virologie, CHU Necker-Enfants Malades, Paris, France. nicole.ngo@nck.ap-hop-paris.fr
authors.forename: N
authors.initials: N
authors.lastname: Ngo-Giang-Huong
authors.forename: C
authors.initials: C
authors.lastname: Deveau
authors.forename: I
authors.initials: I
authors.lastname: Da Silva
authors.forename: I
authors.initials: I
authors.lastname: Pellegrin
authors.forename: A
authors.initials: A
authors.lastname: Venet
authors.forename: M
authors.initials: M
authors.lastname: Harzic
authors.forename: M
authors.initials: M
authors.lastname: Sinet
authors.forename: J F
authors.initials: JF
authors.lastname: Delfraissy
authors.forename: L
authors.initials: L
authors.lastname: Meyer
authors.forename: C
authors.initials: C
authors.lastname: Goujard
authors.forename: C
authors.initials: C
authors.lastname: Rouzioux
mesh_terms: D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D015331:Cohort Studies; D004279:DNA, Viral / Q000097:blood*; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology; D015497:HIV-1; D006801:Humans; D011446:Prospective Studies; D011533:Proviruses; D012367:RNA, Viral / Q000096:biosynthesis / Q000097:blood; D019562:Viral Load; D014779:Virus Replication
chemical_list: D004279:DNA, Viral; D012367:RNA, Viral