title: Virological and immunological effects of salvage therapy following treatment interruption and a shift in HIV-1 resistance genotype.
abstract: The circulating human immunodeficiency virus type 1 (HIV-1) population of patients in whom many prior therapy regimens have failed often undergo a shift from a drug-resistant virus to a wild-type virus following interruption of treatment. This study analyses the virological and immunological effects of salvage therapy following treatment interruption and a shift from a drug-resistance genotype. Twenty-one HIV-1 infected patients who had genotype reversion by population-based sequencing after 3 months of treatment interruption were given a new salvage regimen consisting of 3-5 drugs selected according to their treatment history. Seven (33%) of 21 patients who had fewer than 200 HIV-1 RNA copies/ml until month 12 were defined as virological responders. Four patients were transient responders and 10 were nonresponders. The virological responders were more frequently CDC group A and had higher CD4 + T lymphocyte counts at the time of treatment resumption. The peripheral blood T CD4 + and T CD8 + lymphocyte populations of the patients declined significantly during treatment interruption. Only virological responders showed significant increases in their CD4 + T lymphocyte count 12 months after treatment resumption and these counts rapidly returned to pre-interruption baseline values in most of these patients. Treatment interruption could be useful for optimising salvage therapy for patients previously given many failing regimens. However, controlled trials are needed to assess the clinical benefit of this strategy.
authors.affiliation: Laboratoire de Virologie, Hôpital Purpan, CHU Toulouse, Place du Dr Baylac, Toulouse, France. izopet@cict.fr
authors.forename: Jacques
authors.initials: J
authors.lastname: Izopet
authors.forename: Corinne
authors.initials: C
authors.lastname: Souyris
authors.forename: Karine
authors.initials: K
authors.lastname: Sandres-Sauné
authors.forename: Bénédicte
authors.initials: B
authors.lastname: Puissant
authors.forename: Martine
authors.initials: M
authors.lastname: Obadia
authors.forename: Christophe
authors.initials: C
authors.lastname: Pasquier
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Puel
authors.forename: Antoine
authors.initials: A
authors.lastname: Blancher
authors.forename: Patrice
authors.initials: P
authors.lastname: Massip
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000008:administration & dosage* / Q000494:pharmacology / Q000627:therapeutic use; D018791:CD4 Lymphocyte Count; D018414:CD8-Positive T-Lymphocytes; D004334:Drug Administration Schedule; D024882:Drug Resistance, Viral / Q000235:genetics; D004359:Drug Therapy, Combination; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D006801:Humans; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D018894:Reverse Transcriptase Inhibitors / Q000008:administration & dosage* / Q000494:pharmacology / Q000627:therapeutic use; D016879:Salvage Therapy
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral; D018894:Reverse Transcriptase Inhibitors