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MINI-SYMPOSIUM DE L’IPBS Département « Tuberculose et Biologie des Infections » "Interferons and HIV infection: from protection to disease” MARDI 2 MAI A PARTIR DE 10H Salle des séminaires, CNRS Campus, 205 route de Narbonne – TOULOUSE Acquired immune deficiency syndrome (AIDS) is among the three deadliest diseases due to a single infectious agent. A significant challenge in the AIDS epidemic is to better characterise the innate and humoral antiviral responses, including the regulation of type I interferon signalling. In this minisymposium, two world-renown scientists from the Pasteur institute will expose the latest work from their respective laboratories addressing some of these issues. 10H00 – 11H00 Dr Sandra Pellegrini Institut Pasteur, Paris “ Dysregulation of the type I interferon response, from in vitro studies to human disease ” 11H00 – 12H00 Dr Olivier Schwartz Institut Pasteur, Paris “ HIV spread, innate and humoral antiviral responses ” Contact : Geanncarlo Lugo & Christel Verollet, [email protected] & [email protected] Note for visitors: Please come with a valid identity card Campus CNRS, 205 route de Narbonne TOULOUSE Dr. Sandra Pellegrini Institut Pasteur, Paris Dysregulation of the type I interferon response, from in vitro studies to human disease Type I interferons (IFN-α/β) contribute to innate defense against viruses and regulate homeostasis, differentiation and function of a variety of cell lineages by inducing the transcription of hundreds of genes. Hence, IFN contribute to development of adaptive antimicrobial and antitumor immunity. The action of IFN is rapid but transient and highly controlled. Excess IFN production or a persistent response to IFN can lead to pathogenic processes. We study the regulation of IFN signaling and in particular the role of USP18, an essential negative feedback regulator, which is also an ISG15-specific deconjugating enzyme. I will focus on USP18 and ISG15 function in health and disease and on differences between humans and mice. References Francois-Newton et al. 2011. USP18-based negative feed-back control is induced by Type I and Type III Interferons and specifically inactivates interferons α response. PLOS One 6(7): e22200 Francois-Newton et al. 2012. USP18 establishes the transcriptional and anti-proliferative interferon α/β differential. Biochem J 446:509 Zhang et al. 2015. Human intracellular ISG15 prevents IFN-α/β over-amplification and autoinflammation. Nature 517:89 Meuwissen et al. 2016. Human USP18 deficiency underlies type 1 interferonopathy leading to severe pseudo-TORCH syndrome. J Exp Med 213: 1163 Speer et al. 2016. ISG15 deficiency and increased viral resistance in humans but not mice. Nat Commun 7:11496 Contact : Geanncarlo Lugo & Christel Verollet, [email protected] & [email protected] Note for visitors: Please come with a valid identity card Campus CNRS, 205 route de Narbonne – TOULOUSE Dr. Olivier Schwartz Institut Pasteur, Paris HIV spread, innate and humoral antiviral responses The HIV/AIDS epidemic represents more than ever a public health threat worldwide. About 35 million people are living with HIV/AIDS as of the end of 2014, most of them originating from emerging countries. Our work focuses on cellular and molecular aspects of HIV-1 replication, and on the mechanisms of recognition of HIV-infected cells by the immune system. Specifically, we are interested in studying cell-to-cell spread, which represents a potent and rapid model of viral propagation. Moreover, we intend to better characterize the innate and humoral antiviral responses. In this presentation, I will provide the latest work from our group concerning these key aspects in HIV research. References Descours B et al. CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replication-competent proviruses. Nature 2017 March Compton AA and Schwartz O. They might be giants: Does syncytium formation sink or spread HIV infection?" PLOS Pathog 2017 13(2):e1006099 Bruel T et al. Lack of ADCC breadth of human non-neutralizing anti-HIV-1 antibodies. J Virol 2017 Jan Bruel T et al. Elimination of HIV-1-infected cells by broadly neutralizing antibodies. Nat Commun 2016 7:10844 Donahue DA and Schwartz O. Actin’ on HIV: how dendritic cells spread infection. Cell Host Microbe 2016 19(3):267-9 Contact : Geanncarlo Lugo & Christel Verollet, [email protected] & [email protected] Note for visitors: Please come with a valid identity card Campus CNRS, 205 route de Narbonne – TOULOUSE