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Transcript
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
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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