Journal
JOURNAL OF VIROLOGY
Volume 87, Issue 16, Pages 8862-8869Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.03544-12
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Funding
- Ministry of Health, Labor, and Welfare of Japan
- ERATO (Japan Science and Technology Agency)
- Public Health Service research grants from the National Institute of Allergy and Infectious Diseases
- Japan Society for the Promotion of Science
- Uehara Memorial Foundation
- Senri Life Science Foundation
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [23510254] Funding Source: KAKEN
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Ebola virus (EBOV) protein L (EBOL) acts as a viral RNA-dependent RNA polymerase. To better understand the mechanisms underlying the transcription and replication of the EBOV genome, we sought to identify cellular factors involved in these processes via their coimmunoprecipitation with EBOL and by mass spectrometry. Of 65 candidate proteins identified, we focused on DNA topoisomerase 1 (TOP1), which localizes to the nucleus and unwinds helical DNA. We found that in the presence of EBOL, TOP1 colocalizes and interacts with EBOL in the cytoplasm, where transcription and replication of the EBOV genome occur. Knockdown of TOP1 markedly reduced virus replication and viral polymerase activity. We also found that the phosphodiester bridge-cleaving and recombination activities of TOP1 are required for the polymerase activity of EBOL. These results demonstrate that TOP1 is an important cellular factor for the transcription and replication of the EBOV genome and, as such, plays a key role in the EBOV life cycle.
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