The purpose of this program is to provide stateoftheart postdoctoral training in basic research directed at understanding the mechanisms of virus infection and disease in the central nervous system. The program brings together a faculty of 9 established and wellfunded scientists with the common interest of understanding the consequences of virus infection of the CNS in a wide variety of viral systems. The intent is to prepare highly competent and independent researchers that are wellversed in molecular and cell biology and that possess skills and knowledge sufficient to develop productive independent programs in the area of neurovirology. The career development of the trainees will be facilitated by a training program that provides 1) fulltime research experience under the guidance of experienced senior scientists, 2) instruction in the use of stateoftheart equipment and technologies, 3) an intellectual environment that provides 45 seminars per week by the Institute staff or invited speakers, with opportunities to meet with visiting scientists and faculty members and exchange ideas in neurovirology and related fields, 4) opportunity for formal studies in neurobiology, molecular biology, virology, and immunology; and 5) the opportunity for fellows to present their own research findings for critique by other fellows and staff scientists at least once a year. Trainees will be selected from a pool of qualified M.D., Ph.D., and D.V.M. applicants on the basis of 1) previous Academic and investigative performance, 2) evidence of commitment to biomedical research, in particular to virus diseases of the CNS, and 3) recommendations from previous mentors. Appointments will be for a minimum of two years, with three years as the norm.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Institutional National Research Service Award (T32)
Project #
5T32NS041219-04
Application #
6766799
Study Section
NST-2 Subcommittee (NST)
Program Officer
Nunn, Michael
Project Start
2001-07-15
Project End
2006-06-30
Budget Start
2004-07-01
Budget End
2005-06-30
Support Year
4
Fiscal Year
2004
Total Cost
$315,900
Indirect Cost
Name
Scripps Research Institute
Department
Type
DUNS #
781613492
City
La Jolla
State
CA
Country
United States
Zip Code
92037
Walsh, Kevin B; Teijaro, John R; Brock, Linda G et al. (2014) Animal model of respiratory syncytial virus: CD8+ T cells cause a cytokine storm that is chemically tractable by sphingosine-1-phosphate 1 receptor agonist therapy. J Virol 88:6281-93
Teijaro, John R; Ng, Cherie; Lee, Andrew M et al. (2013) Persistent LCMV infection is controlled by blockade of type I interferon signaling. Science 340:207-11
Walsh, Kevin B; Sidney, John; Welch, Megan et al. (2013) CD8+ T-cell epitope mapping for pneumonia virus of mice in H-2b mice. J Virol 87:9949-52
Oldstone, Michael B A; Teijaro, John R; Walsh, Kevin B et al. (2013) Dissecting influenza virus pathogenesis uncovers a novel chemical approach to combat the infection. Virology 435:92-101
Sullivan, Brian M; Welch, Megan J; Lemke, Greg et al. (2013) Is the TAM receptor Axl a receptor for lymphocytic choriomeningitis virus? J Virol 87:4071-4
Walsh, Kevin B; Teijaro, John R; Zuniga, Elina I et al. (2012) Toll-like receptor 7 is required for effective adaptive immune responses that prevent persistent virus infection. Cell Host Microbe 11:643-53
Kemball, Christopher C; Flynn, Claudia T; Hosking, Martin P et al. (2012) Wild-type coxsackievirus infection dramatically alters the abundance, heterogeneity, and immunostimulatory capacity of conventional dendritic cells in vivo. Virology 429:74-90
Zhang, Adrianna P P; Bornholdt, Zachary A; Liu, Tong et al. (2012) The ebola virus interferon antagonist VP24 directly binds STAT1 and has a novel, pyramidal fold. PLoS Pathog 8:e1002550
Patti, Gary J; Yanes, Oscar; Shriver, Leah P et al. (2012) Metabolomics implicates altered sphingolipids in chronic pain of neuropathic origin. Nat Chem Biol 8:232-4
Teijaro, John R; Walsh, Kevin B; Cahalan, Stuart et al. (2011) Endothelial cells are central orchestrators of cytokine amplification during influenza virus infection. Cell 146:980-91

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