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.
|Lee, Yu-Na; Hwang, Hye Suk; Kim, Min-Chul et al. (2015) Recombinant influenza virus expressing a fusion protein neutralizing epitope of respiratory syncytial virus (RSV) confers protection without vaccine-enhanced RSV disease. Antiviral Res 115:8-Jan|
|Ko, Eun-Ju; Kwon, Young-Man; Lee, Jong Seok et al. (2015) Virus-like nanoparticle and DNA vaccination confers protection against respiratory syncytial virus by modulating innate and adaptive immune cells. Nanomedicine 11:99-108|
|Kwon, Young-Man; Hwang, Hye Suk; Lee, Jong Seok et al. (2014) Maternal antibodies by passive immunization with formalin inactivated respiratory syncytial virus confer protection without vaccine-enhanced disease. Antiviral Res 104:1-6|
|Lee, Sujin; Quan, Fu-Shi; Kwon, Youngman et al. (2014) Additive protection induced by mixed virus-like particles presenting respiratory syncytial virus fusion or attachment glycoproteins. Antiviral Res 111:129-35|
|Meng, Jia; Lee, Sujin; Hotard, Anne L et al. (2014) Refining the balance of attenuation and immunogenicity of respiratory syncytial virus by targeted codon deoptimization of virulence genes. MBio 5:e01704-14|
|Meng, Jia; Stobart, Christopher C; Hotard, Anne L et al. (2014) An overview of respiratory syncytial virus. PLoS Pathog 10:e1004016|
|Wong, Terianne M; Boyapalle, Sandhya; Sampayo, Viviana et al. (2014) Respiratory syncytial virus (RSV) infection in elderly mice results in altered antiviral gene expression and enhanced pathology. PLoS One 9:e88764|
|Dulek, Daniel E; Newcomb, Dawn C; Toki, Shinji et al. (2014) STAT4 deficiency fails to induce lung Th2 or Th17 immunity following primary or secondary respiratory syncytial virus (RSV) challenge but enhances the lung RSV-specific CD8+ T cell immune response to secondary challenge. J Virol 88:9655-72|
|Zhou, Weisong; Goleniewska, Kasia; Zhang, Jian et al. (2014) Cyclooxygenase inhibition abrogates aeroallergen-induced immune tolerance by suppressing prostaglandin I2 receptor signaling. J Allergy Clin Immunol 134:698-705.e5|
|Yan, Dan; Lee, Sujin; Thakkar, Vidhi D et al. (2014) Cross-resistance mechanism of respiratory syncytial virus against structurally diverse entry inhibitors. Proc Natl Acad Sci U S A 111:E3441-9|
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