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Viral reprogramming of host transcription initiation
Nathan A Ungerleider1, Claire Roberts1, Tina M O'Grady1
1Department of Pathology & Laboratory Medicine, Tulane University School of Medicine, Tulane Cancer Center, New Orleans, LA, USA.
Nucleic Acids Research
|March 12, 2024
Summary
Epstein Barr virus (EBV) triggers thousands of new transcription start sites, altering host gene expression. This viral remodeling utilizes a unique viral pre-initiation complex and viral factors, revealing novel virus-host interactions.
Area of Science:
- Virology
- Molecular Biology
- Genomics
Background:
- Viruses reprogram host cells for replication, often by manipulating gene expression.
- Canonical promoters are typically regulated by viral factors during infection.
Purpose of the Study:
- To investigate how Epstein Barr virus (EBV) alters host cell transcription.
- To identify novel transcription start sites and regulatory mechanisms induced by EBV.
Main Methods:
- Genome-wide analysis of transcription initiation sites during EBV replication.
- Characterization of viral pre-initiation complex (vPIC) binding and activity.
- Assessment of viral transcription factors (Zta, Rta) roles in de novo transcription.
Main Results:
- EBV replication induced de novo transcription initiation at 29,674 new start sites.
- A viral pre-initiation complex (vPIC) recognized TATT[T/A]AA sequences, driving transcription.
- Viral factors Zta and Rta influenced de novo promoters, causing transcriptional interference with host promoters.
Conclusions:
- EBV extensively remodels the host transcriptome through widespread de novo transcription.
- Viral factors and unique complexes mediate this transcriptional reprogramming, inhibiting host gene expression.
- These findings offer insights into viral strategies and fundamental eukaryotic promoter function.
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