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Epigenetic Landscape during Coronavirus Infection.
Alexandra Schäfer1, Ralph S Baric2
1Department of Epidemiology, University of North Carolina, Chapel Hill, NC 27599 USA. aschaefe@email.unc.edu.
Pathogens (Basel, Switzerland)
|February 18, 2017
Summary
Emerging coronaviruses (CoV) manipulate host epigenetics to control innate immunity and promote pathogenesis. This study explores viral strategies for epigenome regulation during infection.
Area of Science:
- Virology and Epigenetics
- Molecular Biology
- Immunology
Background:
- Coronaviruses (CoV), including SARS-CoV and MERS-CoV, are significant human and animal pathogens.
- Viral pathogenesis involves complex virus-host interactions affecting entry, replication, egress, and immune control.
- Epigenetics studies how factors alter gene expression without changing DNA sequence, involving modifications like histone alterations and DNA methylation.
Purpose of the Study:
- To investigate the intricate mechanisms by which viruses, particularly pathogenic respiratory RNA viruses, regulate the host epigenome.
- To understand how viruses control host innate immune responses to promote replication and pathogenesis.
- To define novel viral antagonism mechanisms in emerging coronavirus infections.
Main Methods:
- Reviewing strategies for evaluating viral regulation of the host epigenome.
- Focusing on highly pathogenic respiratory RNA virus infections as a model system.
- Integrating epigenome reorganization data with RNA and proteomic datasets.
Main Results:
- Viruses have evolved sophisticated processes to regulate the host epigenome and innate immune defenses.
- A spatial-temporal data integration approach was developed to analyze complex datasets.
- This approach identifies key genomic regions involved in the host's innate immune response.
Conclusions:
- Viruses actively manipulate host epigenetics to evade immune responses and enhance replication.
- Understanding these epigenetic regulatory mechanisms is crucial for developing new antiviral strategies.
- This research defines a new paradigm of viral antagonism in emerging coronavirus infections.
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