7th IAS Conference on HIV Pathogenesis, Treatment and Prevention (IAS 2013)

MOAA01 What Drives Disease Progression and Limits CD4 Recovery?
  Oral Abstract Session : Track A Basic Sciences
Venue: Mini Room 2
Time: 01.07.2013, 14:30 - 16:00
Co-Chairs: Peter Hunt, United States
Irini Sereti, United States

Identification and characterization of CD4 T cells actively transcribing HIV RNA in peripheral blood
J. Casazza, A. Vostel, D. Ambrozak, B. Hill, E. Boritz, D. Douek, R. Koup
Vaccine Research Center, Bethesda, United States

IP10 and sCD163 are biomarkers of CD4+ T cells decline and immune activation in HIV controllers patients
N. Noel1, F. Boufassa2, C. Lécuroux1, A. Saez-Cirion3, I. Girault1, M. Conti4, S. Hua1, C. Bourgeois1, C. Goujard5, A. Venet1, O. Lambotte1,5
1INSERM U 1012, Faculté de Médecine Paris Sud, Le Kremlin Bicêtre, France, 2INSERM U 1018, Faculté de Médecine Paris Sud, Le Kremlin Bicêtre, France, 3Institut Pasteur, Paris, France, 4APHP, Hopital Henri Mondor, Université Paris Est Créteil, Service de Biochimie, Créteil, France, 5AP-HP, Hopital Bicêtre, Université Paris Sud 11, Service de Médecine Interne, Le Kremlin Bicêtre, France

HIV-1 infection reduces emigration of mature thymocytes from the human thymus by downregulation of the sphingosine-1-phosphate receptor S1PR1
R.S. Resop1, M. Douaisi2, J. Craft3, C. Uittenbogaart3
1AIDS Institute at UCLA, Microbiology, Immunology and Molecular Genetics, Los Angeles, United States, 2Rensselaer Polytechnic Institute, Albany, United States, 3AIDS Institute at UCLA, Los Angeles, United States

T cell potential of CD34+ hematopoietic progenitors impact CD4+ T cell recovery under c-ART during HIV infection
I. Menkova1, C. Benne1, Y. Lévy1,2,3, J.-D. Lelièvre1,3,4
1INSERM, U955, Créteil, France, 2APHP, GHU Henri-Mondor, Créteil, France, 3Vaccine Research Institute, Créteil, France, 4Assistance Publique Hopitaux de Paris, Créteil, France

Impaired isotype switching of IgG antibodies in HIV infection may be related to peripheral T-follicular helper cell dysfunction
L. Abudulai1, S. Fernandez1, J. Post2, A. Lloyd2,3, M. French1,4
1The University of Western Australia, School of Pathology and Laboratory Medicine, Perth, Australia, 2Prince of Wales Hospital, Department of Infectious Diseases, Sydney, Australia, 3University of New South Wales, School of Medical Sciences, Sydney, Australia, 4Royal Perth Hospital and Pathwest Laboratory Medicine WA, Department of Clinical Immunology, Perth, Australia

Moderated discussion

Rapporteur report

Track A report by Clovis Steve Palmer

The session ‘What Drives Disease Progression and Limits CD4Recovery’ highlighted major obstacles in understanding  CD4 T cell loss during HIV infection andpotential mechanisms involved in immune reconstitution during cART.

Richard Koup (NIH, Bethesda) presented work that describes the identification of cells within the peripheral blood that actively transcribe HIV.  This is critical for cure strategies. He identifies a subset of low frequency cells called ‘CD4 null’ that had high viral RNA transcription. This was a highlight presentation with some unique assays and analysis methodologies. However,  the mechanism of CD4 down regulation of these infected cells remains to be determined.

Olivier Lambotte (University Paris South) did across-sectional comparison of plasma levels of cytokine and chemokines in Healthy donors, HIV elite controllers, viremic untreated and  HAART teated patients. Interesting data was presented which showed increased inflammatory markers (IP-10 and soluble CD163) in the serum of  elite controllers which may have implications in treatment administration for these patients.

Rachel Resop (AIDS Institute, UCLA) demonstrated  that S1PR1 is upregulated in mature thymocytes that are about to egress the thymus. She proposed that this SIP1 receptor could be a target for therapeutic intervention for the regeneration of CD4+ T cells. This could have implication for non-immunological responders to therapy. 

Inna Menkova  (INSERM, Paris) demonstrated that the  T/NK precursor potential from circulating CD34+ cells is decreased in poor responders (PR) to therapy. A comment from the audience was that the classification of PR and good recovery (good responders) was quite broad and the data could be more informative by a more stringent classification approach.

Laila Abudulia (University of Western Australia) showed that HIV patients irrespective of treatment status had impaired ability  to produce isotype switched IgG antibodies after vaccination with pneumococcal polysaccharides. She correlated response to vaccination with peripheral T-follicular helper (TFH) cells. Whether the phenotypic analysis of these cells in the periphery is a reliable surrogate of TFH in the lymph node is yet to be determined. 


    The organizers reserve the right to amend the programme.