title: Type I interferon production is profoundly and transiently impaired in primary HIV-1 infection.
abstract: BACKGROUND
  Successful immunological control of human immunodeficiency virus (HIV) infection is achieved only in rare individuals. Plasmacytoid dendritic cells (DCs) are mostly responsible for the production of strong antiviral factors--that is, type I interferons (IFNs)--in response to viruses. Their natural IFN production is impaired in chronic HIV infection, in correlation with viral load and disease progression, but it has not been tested during the critical stage of primary infection, when a balance is set between host immune responses and viral replication.
  
  
  METHODS
  We longitudinally studied 26 patients during the primary stage of HIV infection. Fifteen patients received highly active antiretroviral therapy (HAART) for 12 months.
  
  
  RESULTS
  At the time of inclusion into the cohort, median type I IFN production in response to herpes simplex virus type 1 stimulation was dramatically impaired in peripheral blood mononuclear cells (PBMCs) from HIV-infected patients, compared with that in PBMCs from 31 uninfected donors (180 vs. 800 IU/mL; P<.0001). Median circulating plasmacytoid DC counts were also significantly decreased (7300 vs. 13,500 cells/mL; P=.001). Twelve months later, IFN production returned to normal, and the data suggest that HAART may help in the recovery of IFN production by plasmacytoid DCs.
  
  
  CONCLUSIONS
  These data underline the potential for early antiretroviral treatment and IFN- alpha treatment to enhance viral control in a larger proportion of patients during the critical stage of primary infection.
authors.affiliation: Institut Cochin, Département d'Immunologie, INSERM U567, Centre National de la Recherche Scientifique, UMR 8104, IFR 116, Université Paris V René Descartes, France.
authors.forename: Isabelle
authors.initials: I
authors.lastname: Kamga
authors.forename: Sandrine
authors.initials: S
authors.lastname: Kahi
authors.forename: Leyla
authors.initials: L
authors.lastname: Develioglu
authors.forename: Miriam
authors.initials: M
authors.lastname: Lichtner
authors.forename: Concepción
authors.initials: C
authors.lastname: Marañón
authors.forename: Christiane
authors.initials: C
authors.lastname: Deveau
authors.forename: Laurence
authors.initials: L
authors.lastname: Meyer
authors.forename: Cécile
authors.initials: C
authors.lastname: Goujard
authors.forename: Pierre
authors.initials: P
authors.lastname: Lebon
authors.forename: Martine
authors.initials: M
authors.lastname: Sinet
authors.forename: Anne
authors.initials: A
authors.lastname: Hosmalin
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000097:blood / Q000188:drug therapy / Q000821:virology*; D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D015331:Cohort Studies; D003713:Dendritic Cells / Q000276:immunology; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy / Q000821:virology*; D015497:HIV-1; D006801:Humans; D007370:Interferon Type I / Q000096:biosynthesis*; D008137:Longitudinal Studies; D008875:Middle Aged
chemical_list: D007370:Interferon Type I