HIV Research for Prevention: HIVR4P

28.10.14 - 31.10.14



HIV R4P brings more than 1300 of the world's leading prevention researchers, funders and policy makers for four days of exchange, debate and direction-setting for the field. The conference features:



  • 722 abstract presentations (177 oral, 545 posters. The oral and poster counts include 29 poster discussions 65 late-breakers);
  • 4 plenary, and 17 symposia and roundtable sessions;
  • 300 international scholarships; five New Investigator Awardees;
  • Webcasts of all oral sessions– available within 24 hours;
  • An electronic archive of posters (ePosters);
  • 12 satellite sessions;
  • Networking lunches with experts in the field.








Publicaciones o ponencias relacionadas con el congreso

  • 29/10/2014 - Poster A-671-0028-00453 | TRIM5α improves CD8+ T-cell antiviral activity and synergize intrinsic restriction and adaptive immunity in HIV-1 infected cells

    Wednesday, 29 October | Poster P24.11 See more

    Esther Jimenez1, Henrik Kloverpis2, Ruth Peña1, Nuria Izquierdo-Useros1, Bonaventura Clotet1, Philip Goulder2, Greg Towers3 and Julia G. Prado1


    1 AIDS Research Institute –IrsiCaixa-, Hospital Germans Trias i Pujol, Badalona, Spain, 2 Department of Paediatrics, University of Oxford, Peter Medawar Building, OX1 3SY, United Kingdom, 3 Medical Research Council Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, London, United Kingdom.


    Background: TRIM5α restricts HIV-1 replication in a species-specific manner. Its unusual potency is based on association with the incoming viral capsid inducing proteasome dependent premature uncoating. The role of adaptive immunity in restriction by TRIM5α remains uncharacterised, but is crucial to understanding anti-HIV-1 protective immunity. Here, we aim to investigate how TRIM5α might contribute to adaptive immunity against HIV-1.


    Methods: Control U937-HLA-B*27:05 cell lines (E) and stable U937-HLA-B*27:05 expressing rhesus TRIM5α (TRIM5rh) or owl monkey TRIM (TRIMCyp) were generated by transduction. Kinetics of HIV-1 uptake and restriction were measured in all cell lines after infection with HIV-1/VSV, encoding GFP. HIV-1 uptake was measured by p24 staining and virus restriction by enumerating GFP+ cells. To evaluate the effect of TRIM5α on CD8+ T-cell antiviral activity E, TRIM5rh or TRIMCyp expressing cells were infected with HIV-1/VSV and co-cultured with HLA-B*27:05 HIV-1 specific CD8+ T-cells. Relative HIV-1 CD8+ T-cell antiviral activity was quantified, by enumerating GFP+ cells, and killing by live/death expression in co-cultures.


    Results: These experiments revealed accumulation of p24 in TRIM5rh or TRIMCyp cells as compared to control cells (E) (17,3%; 13% and 8,7% respectively). In addition, p24 levels inversely correlated with GFP positivity (Spearman, p=0.026), indicating an association between HIV-1 recruitment and TRIM5α restriction. Our data also show how TRIM5α can significantly increased CD8+ T-cell antiviral activity in TRIM5rh and TRIMCyp infected cells (E vs. TRIM5rh, p=0.0003; E vs. TRIMCyp, p<0.001). This observation was reinforced by an augmentation of CD8+ mediated T-cell death in TRIM5rh and TRIMCyp infected cells.  


    Conclusions: These data reveal a novel role of TRIM5α acting not only as a restriction factor, but also as an adaptive mediator improving HIV-1 CD8+ T-cell responses.