Uzma Hasan
  • E-mail :[email]
  • Phone : +33 04 37 28 24 54
  • Location : Lyon, France
Last update 2019-05-18 00:26:13.141

Uzma Hasan PhD Immunology and Molecular Biology University of London, UK

Course and current status

PI Inserm U1111

Biography: Principle Investigator at the International Center for Infectiology Research (CIRI), Lyon, France, for the last ten years, I have been working in the field of innate immunity. My career path started at Kings College then at St Bart's and Royal London Medical School where I was awarded her PhD in Immunology. My post doctoral training was based at Schering Plough under the direction of Giorgio Trinchieri working in the field of Toll Like Receptors. I worked on HPV, EBV and HBV immune escape from innate receptor sensing. This led to forming ar theme within Inserm in which I continue to understand how chronic infections can prevent innate immune responses.

2016- Immunité innée dans les maladies autoimmunes et infectieuse, CIRI.

Current projects include NK cell exhaustion by HBV, CRISPR Cas9 screens.

2009-2016: Principle Investigator CR1, Inserm U851: Emerging team: Oncoviruses and Innate Immunity. HPV and HBV deregutaion of innate sensing.

2011 : Habilitation a Diriger Les Recherches (HDR) University Claude Bernard Lyon I (UCLB)

2005-2008: Visiting Scientist at International Agency on research for Cancer, Lyon, France. “The role of Toll Like receptors in infectious cancers”.

2001-2004: Scientist at Schering Plough, Lyon, France and Kenilworth, New Jersey, USA. “Toll Like Receptors in HTS: Identification of new TLR agonists for cancer therapy”. 

2000-2001: Research Associate Cytos, Zurich, Switzerland. “HTS Delphi system for identification of new chemokines”.

1997-2001: PhD student St Batholomews and the Royal London Medical School , London, UK; “DNA vaccination for varicella-zoster-virus”.  

1992-1996/7: Program medicine and immunology* at Kings College London, London, UK. * BSc awarded 2.1.

Scientific summary

Oncoviruses and Innate Immunity

Oncoviruses must have the capacity to escape immune surveillance and promote cellular transformation in order to persist and progress in humans. Innate immune responses play a crucial role in the control of viral replication and are required for a timely orchestration of specific adaptive responses against the infection. The innate immune system can sense pathogen components via the Toll Like Receptor (TLR) family and cytosolic receptors. The main objective of our team is to establish a causal role of infectious agents in human cancer and how they affect the innate immune response. We observed that the human papillomavirus type 16 (HPV16) (associated with cervical cancer), a virus that infects the basal epithelium, can effectively deregulate the expression and function of Toll Like Receptor 9 (TLR9) which can sense double-stranded DNA motifs. We will expand our research by elucidating how TLR9 is deregulated by hepatitis B and to examine other double-stranded DNA sensors such as the AIM2 inflammasome are regulated in the context of oncoviral infection. Another ambitious goal will be to determine whether TLR9 has a role in regulating the cell cycle, in particular, to determine the mechanisms that induce events leading to cell death. This highlights a new function of Toll Like Receptors and underscores why TLR9 is targeted by oncoviruses. All studies are conducted in humans and require intensive use of primary human cell cultures, tight collaboration with the CRCL, Lyon, and our data will be corroborated in cohorts of normal and cancerous tissues. In addition, in collaboration with the IARC, Lyon, we seek to examine whether certain polymorphisms in innate receptors will influence the risk of cervical cancer among women in different regions of the world, including France. 

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