title: HIV-1 infection impairs HSV-specific CD4(+) and CD8(+) T-cell response by reducing Th1 cytokines and CCR5 ligand secretion.
abstract: BACKGROUND
  The concept of HIV-1/HSV-negative immunosynergy has recently come to light, which leads us to explore the impact of HIV-1 infection on HSV-specific T-cell immunity.
  
  
  METHODS
  : A combination of interferon (IFN)-γ ELISpot and Luminex-based multicytokine profiling assays was used to compare, in a cross-sectional study, the HSV-specific CD4 and CD8 T-cell responses between 20 HIV-1/HSV-coinfected and 12 HIV-1-uninfected/HSV-infected individuals after in vitro restimulation with HSV glycoprotein D (gD) peptide epitopes.
  
  
  RESULTS
  In response to CD4 and CD8 gD peptide epitopes, mean value (±standard errors of the mean) of the different IFN-γ-secreting T cells (ISC) means was significantly reduced in HIV-1/HSV-coinfected individuals (70 ISC ± 10 and 60 ISC ± 8/10 cells) compared with HIV-1-uninfected/HSV-infected individuals (280 ISC ± 25 and 234 ISC ± 23/10 cells, both P < 0.001). After stimulation with the immunodominant CD4 gD and CD8 gD peptide epitopes, the Th1 cytokine and CCR5 ligand secretions were decreased in the HIV-1-infected group although Th17 cytokines increased. The mean concentration of interleukin (IL)-2, IFN-γ, the IFN-γ-induced protein 10 kDa, and the monokine induced by IFN-γ was correlated to the mean concentration of macrophage inflammatory proteins (MIP-1α, MIP-1β), RANTES and Eotaxin (ρ = 0.56, P = 0.02 and ρ = 0.52, P = 0.03).
  
  
  CONCLUSIONS
  HIV-1 infection impairs both the number and function of HSV-specific T cells. The downregulation of Th1 cytokines and CCR5 ligands in HIV-1/HSV-coinfected individuals may further facilitate both HSV reactivations and HIV-1 replication.
authors.affiliation: Université Montpellier 1, UMR 1058, 34967 Montpellier, France. pierrealainrubbo@gmail.com
authors.forename: Pierre-Alain
authors.initials: PA
authors.lastname: Rubbo
authors.forename: Edouard
authors.initials: E
authors.lastname: Tuaillon
authors.forename: Nicolas
authors.initials: N
authors.lastname: Nagot
authors.forename: Aziz Alami
authors.initials: AA
authors.lastname: Chentoufi
authors.forename: Karine
authors.initials: K
authors.lastname: Bolloré
authors.forename: Jacques
authors.initials: J
authors.lastname: Reynes
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Vendrell
authors.forename: Lbachir
authors.initials: L
authors.lastname: BenMohamed
authors.forename: Philippe
authors.initials: P
authors.lastname: Van De Perre
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism / Q000502:physiology*; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism / Q000502:physiology*; D016207:Cytokines / Q000378:metabolism*; D015536:Down-Regulation; D000939:Epitopes / Q000276:immunology; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000276:immunology* / Q000821:virology; D015497:HIV-1; D006561:Herpes Simplex / Q000150:complications / Q000276:immunology; D006801:Humans; D008024:Ligands; D008297:Male; D008875:Middle Aged; D019713:Receptors, CCR5 / Q000378:metabolism; D018139:Simplexvirus / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D014764:Viral Proteins / Q000276:immunology
chemical_list: D016207:Cytokines; D000939:Epitopes; D008024:Ligands; D019713:Receptors, CCR5; D014764:Viral Proteins