期刊
JOURNAL OF VIROLOGY
卷 84, 期 22, 页码 11888-11897出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01036-10
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资金
- Chinese Ministry of Health [2008ZX 10001-002]
- National Natural Science Foundation of China [31070135, 30900068]
- 973 program [2010CB534907]
- 111 project [B08011]
Viruses are obligate intracellular parasites that depend on cellular machinery for their efficient transcription and replication. In a previous study we reported that bovine foamy virus (BFV) is able to activate the nuclear factor kappa B (NF-kappa B) pathway through the action of its transactivator BTas to enhance viral transcription. However, the mechanism used by NF-kappa B to enhance BFV transcription remains elusive. To address this question, we employed a yeast two-hybrid assay to screen for BTas-interacting proteins. We found that RelB, a member of NF-kappa B protein family, interacts with BTas. We confirmed the putative RelB-BTas interaction in vitro and in vivo and identified the protein regions responsible for the RelB-BTas interaction. Using a luciferase reporter assay, we next showed that RelB enhances BFV transcription (BTas-induced long terminal repeat [LTR] transactivation) and that this process requires both the localization of the RelB-BTas interaction in the nucleus and the Rel homology domain of RelB. The knockdown of the cellular endogenous RelB protein using small interfering RNA (siRNA) significantly attenuated BTas-induced LTR transcription. The results of chromatin immunoprecipitation (ChIP) analysis showed that endogenous RelB binds to the viral LTR in BFV-infected cells. Together, these results suggest that BFV engages the RelB protein as a cotransactivator of BTas to enhance viral transcription. In addition, our findings indicate that BFV infection upregulates cellular RelB expression through BTas-induced NF-kappa B activation. Thus, this study demonstrates the existence of a positive-feedback circuit in which BFV utilizes the host's NF-kappa B pathway through the RelB protein for efficient viral transcription.
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