Bulletin of the American Physical Society
APS March Meeting 2017
Volume 62, Number 4
Monday–Friday, March 13–17, 2017; New Orleans, Louisiana
Session E49: DBIO Delbruck Award SessionInvited Prize/Award Undergraduate
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Sponsoring Units: DBIO Chair: Ilya Nemenman, Emory University Room: 396 |
Tuesday, March 14, 2017 8:00AM - 8:36AM |
E49.00001: Exploiting single-cell variability to infer the dynamics of immune responses Invited Speaker: Thomas H\"ofer Cell division, differentiation, migration and death determine the dynamics of immune responses. These processes are regulated by a multitude of biochemical signals which, at present, cannot faithfully be reconstituted outside the living organism. However, quantitative measurements in living organisms have been limited. In recent years experimental techniques for the ``fate mapping'' of single immune cells have been developed that allow performing parallel single-cell experiments in an experimental animal. The resulting data are more informative about underlying biological processes than traditional measurements. I will show how the theory of stochastic dynamical systems can be used to infer the topology and dynamics of cell differentiation pathways from such data. The focus will be on joint theoretical and experimental work addressing: (i) the development of immune cells during hematopoiesis, and (ii) T cell responses to diverse pathogens. I will discuss questions on the nature of cellular variability that are posed by these new findings. [Preview Abstract] |
Tuesday, March 14, 2017 8:36AM - 9:12AM |
E49.00002: Diversity of immune systems. Invited Speaker: Aleksandra Walczak The recognition of pathogens relies on the diversity of immune receptor proteins. Recent experiments that sequence entire immune cell repertoires provide a new opportunity for quantitative insight into naturally occurring diversity and how it is generated. I will show how applying statistical inference to these recent experiments that sequence entire B and T-cell repertoires we can quantify the origins of diversity in these sequences and characterize selection acting on the somatic evolutionary process that leads to the observed receptor diversity. I will finish by showing how the known types of immunity observed in nature can be explained in terms of evolutionary arguments. [Preview Abstract] |
Tuesday, March 14, 2017 9:12AM - 9:48AM |
E49.00003: How to hit HIV where it hurts Invited Speaker: Arup Chakraborty No medical procedure has saved more lives than vaccination. But, today, some pathogens have evolved which have defied successful vaccination using the empirical paradigms pioneered by Pasteur and Jenner. One characteristic of many pathogens for which successful vaccines do not exist is that they present themselves in various guises. HIV is an extreme example because of its high mutability. This highly mutable virus can evade natural or vaccine induced immune responses, often by mutating at multiple sites linked by compensatory interactions. I will describe first how by bringing to bear ideas from statistical physics (e.g., maximum entropy models, Hopfield models, Feynman variational theory) together with in vitro experiments and clinical data, the fitness landscape of HIV is beginning to be defined with explicit account for collective mutational pathways. I will describe how this knowledge can be harnessed for vaccine design. Finally, I will describe how ideas at the intersection of evolutionary biology, immunology, and statistical physics can help guide the design of strategies that may be able to induce broadly neutralizing antibodies. [Preview Abstract] |
Tuesday, March 14, 2017 9:48AM - 10:24AM |
E49.00004: Harnessing transcriptional fluctuations for cell-fate control and therapy Invited Speaker: Leor Weinberger |
Tuesday, March 14, 2017 10:24AM - 11:00AM |
E49.00005: Delbruck Prize Award: Insights into HIV Dynamics and Cure Invited Speaker: Alan S. Perelson A large effort is being made to find a means to cure HIV infection. I will present a dynamical model of a phenomenon called post-treatment control (PTC) or “functional cure” of HIV-infection in which some patients treated with suppressive antiviral therapy have been taken off of therapy and then spontaneously control HIV infection. The model relies on an immune response and bistability to explain PTC. I will then generalize the model to explicitly include immunotherapy with monoclonal antibodies approved for use in cancer to show that one can induce PTC with a limited number of antibody infusions and compare model predictions with experiments in SIV infected macaques given immunotherapy. Lastly, I will argue that quantitative insights derived from models of HIV infection have and will continue to play an important role in medicine. [Preview Abstract] |
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