期刊
CELL
卷 139, 期 7, 页码 1255-1267出版社
CELL PRESS
DOI: 10.1016/j.cell.2009.12.018
关键词
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资金
- National Institutes of Health (NIH) [U01 AI074575, R01 HG001715, P50 HG004233]
- NIH New Innovator Award
- Ford Foundation Predoctoral Fellowship
- EMBO Postdoctoral Fellowship
- The Ellison Foundation
- Howard Hughes Medical Institute
- Burroughs Wellcome Fund
- NIH Pioneer Award
- Sloan Foundation
- [U54 AI057159]
During the course of a viral infection, viral proteins interact with an array of host proteins and pathways. Here, we present a systematic strategy to elucidate the dynamic interactions between H1N1 influenza and its human host. A combination of yeast two-hybrid analysis and genome-wide expression profiling implicated hundreds of human factors in mediating viral-host interactions. These factors were then examined functionally through depletion analyses in primary lung cells. The resulting data point to potential roles for some unanticipated host and viral proteins in viral infection and the host response, including a network of RNA-binding proteins, components of WNT signaling, and viral polymerase subunits. This multilayered approach provides a comprehensive and unbiased physical and regulatory model of influenza-host interactions and demonstrates a general strategy for uncovering complex host-pathogen relationships.
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