The overall goal of the PFS is to stimulate innovative research relevant to mechanisms of viral persistence. This program is one mechanism through which this collaborative Study Group will facilitate the development of young investigators focused on areas relevant to the scientific mission of the HPSG and will encourage basic investigators to extend their studies into chronic viral infections, often in collaboration with members of the HPSG directly focused on these disorders. An important parallel goal is to foster the growth of young investigators, in the hope of increasing the number of workers studying these disorders. It should be emphasized that PFS awards are not designed to serve as "bridge funding" for investigators "between grants" or to support projects with pending support from outside funding agencies. It is anticipated that PFS recipients will lead to further, ongoing research funding by external peer-reviewed agencies as well as results warranting publication in peer-reviewed journals. Three general types of PFS applications will be considered for funding: TYPE I Those from young investigators without current or past independent NIH support establishing research programs relevant to the Aims of the HPSG. Applicants for this type of award generally hold an initial faculty appointment;senior post-doctoral fellows may also apply if there is a documented commitment by their department t a faculty appointment within the PFS support period TYPE II Those from established scientists not currently focused on chronic infection with Emerging Pathogens per se who will extend their studies to encompass issues of direct of indirect importance to understanding chronic viral infection TYPE III Those from investigators with novel projects distinctly removed from their established research program. All members of the participant HPSG institutions are eligible to receive funding through the PFS program. They are expected to attend HPSG seminars, interact with other center investigators and present their findings to the members of the HPSG in addition to formal reporting to the Executive Committee as described below. While the goals of the PFS program encompasses the three types of applications noted above, TYPE I proposals have highest priority. An investigator may not receive more than one PFS award during the HPSG grant period.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
5U19AI082630-05
Application #
8475552
Study Section
Special Emphasis Panel (ZAI1-KS-I)
Project Start
Project End
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
5
Fiscal Year
2013
Total Cost
$193,402
Indirect Cost
$51,320
Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199
Lin, Wenyu; Zhu, Chuanlong; Hong, Jian et al. (2015) The spliceosome factor SART1 exerts its anti-HCV action through mRNA splicing. J Hepatol 62:1024-32
Jilg, Nikolaus; Lin, Wenyu; Hong, Jian et al. (2014) Kinetic differences in the induction of interferon stimulated genes by interferon-* and interleukin 28B are altered by infection with hepatitis C virus. Hepatology 59:1250-61
Kroy, Daniela C; Ciuffreda, Donatella; Cooperrider, Jennifer H et al. (2014) Liver environment and HCV replication affect human T-cell phenotype and expression of inhibitory receptors. Gastroenterology 146:550-61
Lee, Mark N; Ye, Chun; Villani, Alexandra-ChloƩ et al. (2014) Common genetic variants modulate pathogen-sensing responses in human dendritic cells. Science 343:1246980
Crawford, Alison; Angelosanto, Jill M; Kao, Charlly et al. (2014) Molecular and transcriptional basis of CD4? T cell dysfunction during chronic infection. Immunity 40:289-302
Feeney, Eoin R; Chung, Raymond T (2014) Antiviral treatment of hepatitis C. BMJ 348:g3308
Fackler, Oliver T; Murooka, Thomas T; Imle, Andrea et al. (2014) Adding new dimensions: towards an integrative understanding of HIV-1 spread. Nat Rev Microbiol 12:563-74
Xiao, Yanping; Yu, Sanhong; Zhu, Baogong et al. (2014) RGMb is a novel binding partner for PD-L2 and its engagement with PD-L2 promotes respiratory tolerance. J Exp Med 211:943-59
Veerapu, Naga Suresh; Park, Su-Hyung; Tully, Damien C et al. (2014) Trace amounts of sporadically reappearing HCV RNA can cause infection. J Clin Invest 124:3469-78
Ussher, James E; Bilton, Matthew; Attwod, Emma et al. (2014) CD161++ CD8+ T cells, including the MAIT cell subset, are specifically activated by IL-12+IL-18 in a TCR-independent manner. Eur J Immunol 44:195-203

Showing the most recent 10 out of 72 publications