CORE A: Given the size, complexity, duration, and scope involved. Core A will be fundamental in enabling the successful establishment and operation of the entire program. All costs for administrative support for the Cores and Projects are included here. Dr. Stokes Peebles will assume ultimate administrative responsibility for the management of this Core. Administrative, fiscal services, and clerical support for the entire program will be shared by all Project Leaders, Core Leaders and Co-Investigators. This Core will provide and maintain all of the administrative space and functions for the entire program, including but not limited to, offices for all investigators, an administrative area with secretarial and administrative support, a copy/work room, and a conference room with up to date audiovisual amenities. Administrative functions will include ordering of supplies and equipment, maintenance of all records, keeping and monitoring of budgets, maintenance of the personnel database for grant effort, interactions with University administrative offices and the NIH regarding budgetary and other administrative matters, and scheduling and organizing meetings and presentations. This Core will support all of the computer hardware and software resources for the administrative and clerical functions of the program. This Core will coordinate and support the activities of the Internal Advisory Committee and the External Scientific Advisory Board. The basic functions and objectives of the Core include: quality management of program resources, integration of the program, oversight of deliverables within the timeframe, assistance with data management, and leading the vision. To achieve these objectives, detailed plans are presented for administrative structure and leadership, project management, external Scientific Advisory Board, and communication/meetings.
RSV is the leading cause of bronchiolitis and causes >100,000 infant hopsitalizations in the US each year. Studies have also revealed that severe RSV infection in infancy is associated with the later development of childhood asthma. This application will examine both host genetic and immune response determinants, as well as the influence of specific RSV strains, on severity of RSV bronchiolitis and childhood asthma. In addition, we will define the role of a novel therapeutic target, PGI2, in RSV pathogenesis.
|Shilts, Meghan H; Rosas-Salazar, Christian; Tovchigrechko, Andrey et al. (2016) Minimally Invasive Sampling Method Identifies Differences in Taxonomic Richness of Nasal Microbiomes in Young Infants Associated with Mode of Delivery. Microb Ecol 71:233-42|
|Mathias, Rasika Ann; Taub, Margaret A; Gignoux, Christopher R et al. (2016) A continuum of admixture in the Western Hemisphere revealed by the African Diaspora genome. Nat Commun 7:12522|
|Rosas-Salazar, Christian; Shilts, Meghan H; Tovchigrechko, Andrey et al. (2016) Nasopharyngeal Microbiome in Respiratory Syncytial Virus Resembles Profile Associated with Increased Childhood Asthma Risk. Am J Respir Crit Care Med 193:1180-3|
|Rostad, Christina A; Stobart, Christopher C; Gilbert, Brian E et al. (2016) A Recombinant Respiratory Syncytial Virus Vaccine Candidate Attenuated by a Low-Fusion F Protein Is Immunogenic and Protective against Challenge in Cotton Rats. J Virol 90:7508-18|
|Lee, Sujin; Nguyen, Minh Trang; Currier, Michael G et al. (2016) A polyvalent inactivated rhinovirus vaccine is broadly immunogenic in rhesus macaques. Nat Commun 7:12838|
|Stobart, Christopher C; Rostad, Christina A; Ke, Zunlong et al. (2016) A live RSV vaccine with engineered thermostability is immunogenic in cotton rats despite high attenuation. Nat Commun 7:13916|
|Tan, Yi; Hassan, Ferdaus; Schuster, Jennifer E et al. (2016) Molecular Evolution and Intraclade Recombination of Enterovirus D68 during the 2014 Outbreak in the United States. J Virol 90:1997-2007|
|Banathy, Alex; Cheung-Flynn, Joyce; Goleniewska, Kasia et al. (2016) Heat Shock-Related Protein 20 Peptide Decreases Human Airway Constriction Downstream of Î²2-Adrenergic Receptor. Am J Respir Cell Mol Biol 55:225-33|
|Zhou, Weisong; Zhang, Jian; Goleniewska, Kasia et al. (2016) Prostaglandin I2 Suppresses Proinflammatory Chemokine Expression, CD4 T Cell Activation, and STAT6-Independent Allergic Lung Inflammation. J Immunol 197:1577-86|
|Stier, Matthew T; Bloodworth, Melissa H; Toki, Shinji et al. (2016) Respiratory syncytial virus infection activates IL-13-producing group 2 innate lymphoid cells through thymic stromal lymphopoietin. J Allergy Clin Immunol 138:814-824.e11|
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