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B and IFN-Regulatory Factor Transcription Factors1
Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, and Departments of Microbiology and Immunology, Medicine and Oncology, McGill University, Montreal, Canada
Virus infection of host cells activates a set of cellular genes,
including cytokines, IFNs, and chemokines, involved in antiviral
defense and immune activation. Previous studies demonstrated that
virus-induced transcriptional activation of a member of the human
CC-chemokine RANTES required activation of the latent transcription
factors IFN-regulatory factor (IRF)-3 and NF-
B via posttranslational
phosphorylation. In the present study, we further characterized the
regulatory control of RANTES transcription during virus infection using
in vivo genomic footprinting analyses. IRF-3, the related IRF-7, and
NF-B are identified as important in vivo binding factors required
for the cooperative induction of RANTES transcription after virus
infection. Using fibroblastic or myeloid cells, we demonstrate that the
kinetics and strength of RANTES virus-induced transcription are highly
dependent on the preexistence of IRFs and NF-B. Use of dominant
negative mutants of either IB-
or IRF-3 demonstrate that
disruption of either pathway dramatically abolishes the ability of the
other to bind and activate RANTES expression. Furthermore, coexpression
of IRF-3, IRF-7, and p65/p50 leads to synergistic activation of RANTES
promoter transcription. These studies reveal a model of virus-mediated
RANTES promoter activation that involves cooperative synergism between
IRF-3/IRF-7 and NF-B factors.
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