OBJECTIVE: Expansion of regulatory T (Treg) cells has been described in chronically HIV-infected individuals. We investigated whether HIV-suppressive Treg could be detected during primary HIV infection (PHI). METHODS: Seventeen patients diagnosed early after PHI (median: 13 days; 1-55) were studied. Median CD4 cell count was 480 cells/microl (33-1306) and plasma HIV RNA levels ranged between 3.3 and 5.7 log10 copies/ml. Suppressive capacity of blood purified CD4CD25 was evaluated in a coculture assay. Fox-p3, IL-2 and IL-10 were quantified by reverse transcriptase (RT)-PCR and intracellular staining of ex vivo and activated CD4+CD25 T cells. RESULTS: The frequency of CD4CD127CD25 T cells among CD4 T cells was lower in patients with PHI compared with chronic patients (n = 19). They exhibited a phenotype of memory T cells and expressed constitutively FoxP3. Similar to chronic patients, Treg from patients with PHI inhibited the proliferation of purified tuberculin (PPD) and HIV p24 activated CD4CD25 T cells. CD4CD25 T cells from patients with PHI responded specifically to p24 stimulation by expressing IL-10. In untreated patients with PHI, the frequency as well as HIV-specific activity of Treg decreased during a 24-month follow-up. A positive correlation between percentages of Treg and both CD4 cell counts and the magnitude of p24-specific suppressive activity at diagnosis of PHI was found. CONCLUSION: Our data showed that HIV drives Treg, as PHI and these cells persist throughout the course of the infection. A correlation between the frequency of Treg and CD4 T-cell counts suggest that these cells may impact on the immune activation set point at PHI diagnosis.
OBJECTIVE: Expansion of regulatory T (Treg) cells has been described in chronically HIV-infected individuals. We investigated whether HIV-suppressive Treg could be detected during primary HIV infection (PHI). METHODS: Seventeen patients diagnosed early after PHI (median: 13 days; 1-55) were studied. Median CD4 cell count was 480 cells/microl (33-1306) and plasma HIV RNA levels ranged between 3.3 and 5.7 log10 copies/ml. Suppressive capacity of blood purified CD4CD25 was evaluated in a coculture assay. Fox-p3, IL-2 and IL-10 were quantified by reverse transcriptase (RT)-PCR and intracellular staining of ex vivo and activated CD4+CD25 T cells. RESULTS: The frequency of CD4CD127CD25 T cells among CD4 T cells was lower in patients with PHI compared with chronic patients (n = 19). They exhibited a phenotype of memory T cells and expressed constitutively FoxP3. Similar to chronic patients, Treg from patients with PHI inhibited the proliferation of purified tuberculin (PPD) and HIV p24 activated CD4CD25 T cells. CD4CD25 T cells from patients with PHI responded specifically to p24 stimulation by expressing IL-10. In untreated patients with PHI, the frequency as well as HIV-specific activity of Treg decreased during a 24-month follow-up. A positive correlation between percentages of Treg and both CD4 cell counts and the magnitude of p24-specific suppressive activity at diagnosis of PHI was found. CONCLUSION: Our data showed that HIV drives Treg, as PHI and these cells persist throughout the course of the infection. A correlation between the frequency of Treg and CD4 T-cell counts suggest that these cells may impact on the immune activation set point at PHI diagnosis.
Authors: Mindi R Walker; Bryan D Carson; Gerald T Nepom; Steven F Ziegler; Jane H Buckner Journal: Proc Natl Acad Sci U S A Date: 2005-03-07 Impact factor: 11.205
Authors: G Pantaleo; J F Demarest; T Schacker; M Vaccarezza; O J Cohen; M Daucher; C Graziosi; S S Schnittman; T C Quinn; G M Shaw; L Perrin; G Tambussi; A Lazzarin; R P Sekaly; H Soudeyns; L Corey; A S Fauci Journal: Proc Natl Acad Sci U S A Date: 1997-01-07 Impact factor: 11.205
Authors: Christopher Kornfeld; Mickaël J-Y Ploquin; Ivona Pandrea; Abdourahmane Faye; Richard Onanga; Cristian Apetrei; Virginie Poaty-Mavoungou; Pierre Rouquet; Jérôme Estaquier; Lorenzo Mortara; Jean-François Desoutter; Cécile Butor; Roger Le Grand; Pierre Roques; François Simon; Françoise Barré-Sinoussi; Ousmane M Diop; Michaela C Müller-Trutwin Journal: J Clin Invest Date: 2005-03-10 Impact factor: 14.808
Authors: J V Giorgi; L E Hultin; J A McKeating; T D Johnson; B Owens; L P Jacobson; R Shih; J Lewis; D J Wiley; J P Phair; S M Wolinsky; R Detels Journal: J Infect Dis Date: 1999-04 Impact factor: 5.226
Authors: Frank O Pettersen; Eirik A Torheim; Anders E A Dahm; Ingeborg S Aaberge; Andreas Lind; Malin Holm; Einar M Aandahl; Per M Sandset; Kjetil Taskén; Dag Kvale Journal: J Virol Date: 2011-04-13 Impact factor: 5.103
Authors: G Degaffe; R Zakhour; W Zhang; G A Contreras; C S Bell; G Rodriguez; G Del Bianco; N Pérez; L J Benjamins; J R Murphy; G P Heresi; D Q Tran Journal: Clin Exp Immunol Date: 2015-04 Impact factor: 4.330
Authors: J Saison; T Ferry; J Demaret; D Maucort Boulch; F Venet; T Perpoint; F Ader; V Icard; C Chidiac; G Monneret Journal: Clin Exp Immunol Date: 2014-06 Impact factor: 4.330
Authors: Adriana Weinberg; Ronald Bosch; Kara Bennett; Adriana Tovar-Salazar; Constance A Benson; Ann C Collier; Andrew Zolopa; Roy M Gulick; David Wohl; Bruce Polsky; Alejo Erice; Mark A Jacobson Journal: J Acquir Immune Defic Syndr Date: 2014-05-01 Impact factor: 3.731