||Multi-Faceted Aspects of Acute HIV Infection
Oral Poster Discussion Session : Track A Basic Sciences
||Mini Room 4
||01.07.2013, 13:00 - 14:00
Christine Rouzioux, France
Anthony Kelleher, Australia
C. Rouzioux, France
|Genetic diversity at endoplasmatic reticulum aminopeptidases 2 (ERAP2) is coupled with resistance to HIV-1 infection|
I. Saulle1, M. Biasin1, M. Sironi2, M. de Luca1, F. la Rosa1, R. Cagliani2, S. lo Caputo3, F. Mazzotta3, M. Clerici1
1University of Milan, Immunology, Segrate, Italy, 2Scientific Institute IRCCS E MEDEA, Bosisio Parini, Italy, 3Hospital Santa Maria Annunziata, Florence, Italy
|Association of APOBEC3G genetic variants with HIV-1vif sequence variation and impact on HIV-1 pathogenesis|
K. Reddy1, M. Ooms2, K. Mlisana3, S. Abdool Karim3, V. Simon2, T. Ndung'u1, CAPRISA Acute Infection Team
1Nelson R. Mandela School of Medicine, University of KwaZulu Natal, HIV Pathogenesis Program, Durban, South Africa, 2Mount Sinai School of Medicine, Department of Microbiology and Global Health and Emerging Pathogens Institute, New York, United States, 3University of KwaZulu-Natal, Centre for the AIDS Programme of Research in South Africa (CAPRISA), Durban, South Africa
|Viral protein U (Vpu) reduces innate sensing of human immunodeficiency virus type 1 (HIV-1)- infected T cells by plasmacytoid dendritic cells (pDCs) via a BST2-dependent process|
M.G. Bego1, É. Bérubé-Côté1, J. Mercier1, É.A. Cohen1,2
1Institut de Recherches Cliniques de Montréal, Laboratory of Human Retrovirology, Montreal, Canada, 2Université de Montréal, Microbiology and Immunology, Montreal, Canada
|ADCC responses arising during acute/early HIV infection do not prevent rapid disease progression|
M.J. Ruiz1, Y. Ghiglione1, M.E. Socías2, N. Laufer1,3, P. Cahn2,3, O. Sued2, M.M. Gherardi1, H. Salomon1, A.M. Rodriguez1, G. Turk1
1Instituto de Investigaciones Biomédicas en Retrovirus y Sida, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina, 2Fundación Huesped, Buenos Aires, Argentina, 3Hospital Juan A. Fernández, Unidad Enfermedades Infecciosas, Buenos Aires, Argentina
|T cell activation positively correlates with cell-associated HIV-DNA level in PBMCs in viremic patients with acute or chronic HIV-1 infection|
L. Weiss1,2, M. Chevalier1, L. Assoumou3, C. Dider1, P.-M. Girard4, D. Costagliola3,5, C. Rouzioux6, ANRS116 SALTO Study Group
1Institut Pasteur, Unité de Régulation des Infections Rétrovirales, Paris, France, 2Université Paris Descartes, Paris, France, 3INSERM U943, Paris, France, 4CHU Saint-Antoine, Paris, France, 5Université Pierre et Marie Curie, Paris, France, 6Université Paris Descartes, EA 3620, Paris, France
A. Kelleher, Australia
|Genetic diversity at endoplasmatic reticulum aminopeptidases 2 (ERAP2) is coupled with resistance to HIV-1 infection - Irma Saulle|
|ADCC responses arising during acute/early HIV infection do not prevent rapid disease progression - María Julia Ruiz|
|T cell activation positively correlates with cell-associated HIV-DNA level in PBMCs in viremic patients with acute or chronic HIV-1 infection - Laurence Weiss|
Track A report by Gabriella Scarlatti
Multi-Faceted Aspects ofAcute HIV Infection.
The acute infection phase is an important step during HIV infection and there is increasing evidence showing that it can predict HIV disease outcome. In this session, several aspects regarding the early events during the primary infection and their implication on the outcome of HIV disease were presented, such as host determinants, host/viral factor interactions, and the early reservoir and immune activation.
I. Saulle presented data showing that the expression of full-length haplotype of ERAP2 (endoplasmic reticulum aminopeptidase 2), in association or not with HLA-B57, confers protection from HIV infection. This enhanced protection may be due to the modulation of the antigen processing and presentation.
K. Reddy presented interesting data of the adaptation of HIV subtype C protein Vif to the APOBEC3G immune pressure. They studied longitudinally blood samples from early HIV infected patients, and analyzed the capacity of the generated vif alleles to counteract APOBEC3G 186H (WT) or 186R (variant 186Ris associated with high viremia). Reddy showed that during early HIV infection there is a selection of vif mutants with a greater capacity to counteract the APOBEC3G 186R (WT).
E. Cohen focused on the involvement of Vpu/BST2 interaction in the response of pDC to HIV-infected CD4+T cells. It is known that BST2 imped the release of HIV virions, and that it is counteracted by Vpu. pDC are possibly sensing HIV attached to the surface of cells rather than free virions. He showed that Vpu can modulate the pDC response to HIV-infected CD4 T cells (measured by IFN I secretion) by promoting the release of HIV viral particles from HIV-infected cells and therefore decreasing the capacity of pDC to detect HIV infection.
Lastly, L. Weiss showed that the levels of Tcell activation positively correlate with cell-associated HIV-DNA levels in viremic patients, whereas no correlation was observed in aviremic ARV treated patients. Further suggesting that the residual immune activation observed in aviremic patients is not directly dependent on the size of HIV reservoir.