Since the inception of the NIH T32-supported University of Washington's Pediatric Infectious Diseases Training Program in 1981, our faculty has trained 92 fellows, 5 of who will be continuing training with the support of this grant. Of the 87 former trainees, 72 (84%) are actively involved in research careers in academic positions at universities (n=58), government (n=5), or industry (n=9). Fellows who have completed training in the past 10 years have had remarkable early success in research careers, with most (n=12/16, 75%) progressing to the NIH K series of awards. Since submission of our last competitive renewal, 11 fellows have completed training in our program, including two individuals from under-represented-minorities. Nine of these 11 (82%) fellows have published one or more (a total of 31, mean 2.8) publications related to their fellowship research in peer- reviewed journals. The objective of our program is to identify and recruit committed young post-doctoral physicians and scientists interested in pediatric infectious diseases. We provide them with training in microbiology, molecular and cellular techniques, genomics, proteomics, bioinformatics, and translational strategies. Under the direction of a senior mentor with a record of successful projects supported by the NIH or foundations, each fellow leads at least one research project during our 3-year fellowship. Integrated into our program is training to perform research with human subjects and animals in compliance with all the federal regulations, grant and manuscript preparation and strategies to succeed in academia. Through our mentoring and training, we aim to propel our fellows to contribute critical insights into understanding and treating pediatric infectious diseases.
Infectious diseases continue to contribute to most deaths in children. Academic researchers focused on infectious diseases have contributed to the elimination or control of many infections that have killed or maimed children, including small pox, polio, meningitis, measles, prevention of pediatric AIDS and diarrhea. Training individuals to continue this work is important to improving the health of the world's children.
|Whidbey, Christopher; Harrell, Maria Isabel; Burnside, Kellie et al. (2013) A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta. J Exp Med 210:1265-81|
|Burnside, Kellie; Rajagopal, Lakshmi (2012) Regulation of prokaryotic gene expression by eukaryotic-like enzymes. Curr Opin Microbiol 15:125-31|
|Little, Malaika L; Qin, Xuan; Zerr, Danielle M et al. (2012) Molecular diversity in mechanisms of carbapenem resistance in paediatric Enterobacteriaceae. Int J Antimicrob Agents 39:52-7|
|Lundgren, Ingrid S; Englund, Janet A; Burroughs, Lauri M et al. (2012) Outcomes and duration of Pneumocystis jiroveci pneumonia therapy in infants with severe combined immunodeficiency. Pediatr Infect Dis J 31:95-7|
|Burnside, Kellie; Rajagopal, Lakshmi (2011) Aspects of eukaryotic-like signaling in Gram-positive cocci: a focus on virulence. Future Microbiol 6:747-61|
|Jaspan, Heather B; Flisher, Alan J; Myer, Landon et al. (2011) Sexual health, HIV risk, and retention in an adolescent HIV-prevention trial preparatory cohort. J Adolesc Health 49:42-6|
|Jaspan, Heather B; Mueller, Alexandra D; Myer, Landon et al. (2011) Effect of caregivers' depression and alcohol use on child antiretroviral adherence in South Africa. AIDS Patient Care STDS 25:595-600|
|Jaspan, Heather B; Liebenberg, Lenine; Hanekom, Willem et al. (2011) Immune activation in the female genital tract during HIV infection predicts mucosal CD4 depletion and HIV shedding. J Infect Dis 204:1550-6|
|Burnside, Kellie; Lembo, Annalisa; Harrell, Maria Isabel et al. (2011) Serine/threonine phosphatase Stp1 mediates post-transcriptional regulation of hemolysin, autolysis, and virulence of group B Streptococcus. J Biol Chem 286:44197-210|
|Gantt, Soren; Carlsson, Jacquelyn; Heath, Laura et al. (2010) Genetic analyses of HIV-1 env sequences demonstrate limited compartmentalization in breast milk and suggest viral replication within the breast that increases with mastitis. J Virol 84:10812-9|
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