models for both the GABA A receptor and 11b-hydroxylase when performing their docking studies. Nevertheless, they were still able to successfully identify compounds that were potent GABA A receptor modulators but lacked significant 11b-hydroxylase inhibitory activity. Recently, Laverty et al. reported the structure of a synaptic GABA A receptor using cryo-electron microscopy [10]. Thus, one could reasonably expect that in silico screening assays utilizing this new structure could provide even more accurate predictions of GABA A receptor modulatory potency and anesthetic activity. In summary, there is a compelling need for new general anesthetics that are devoid of the side effects that risk harm to patients. The work by Cayla and colleagues provides proof-ofconcept for the use of in silico docking approaches to rapidly screen virtual libraries to identify compounds with potent anesthetic activities that are devoid of side effects mediated by off-target sites. We look forward to the day when a novel anesthetic agent first identified by such approaches is available for use in patients.

The CD8 + T cell response is critical to the control of viral infections. Yet, defining the CD8 + T cell response to viral infections quantitatively has been a challenge. Following antigen recognition, which triggers an intracellular signaling cascade, CD8 + T cells can differentiate into effector cells, which proliferate rapidly and destroy infected cells. When the infection is cleared, they leave behind memory cells for quick recall following a second challenge. If the infection persists, the cells may become exhausted, retaining minimal control of the infection while preventing severe immunopathology. These activation, proliferation and differentiation processes as well as the mounting of the effector response are intrinsically multiscale and collective phenomena. Remarkable experimental advances in the recent years, especially at the single cell level, have enabled a quantitative characterization of several underlying processes. Simultaneously, sophisticated mathematical models have begun to be constructed that describe these multiscale phenomena, bringing us closer to a comprehensive description of the CD8 + T cell response to viral infections. Here, we review the advances made and summarize the challenges and opportunities ahead. This article is categorized under: Analytical and Computational Methods > Computational Methods Biological Mechanisms > Cell Fates Biological Mechanisms > Cell Signaling Models of Systems Properties and Processes > Mechanistic Models

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