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Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
Published on: September 13, 2018
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Cellular antibody affinity-based CRISPR screening identifies JUNB as a broadly acting antiviral factor
Nicole C Waild1, Jessica H Ciesla1, Xenia L Schafer1
1Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642.
Summary
A new CRISPR screening pipeline called VIRCAA identifies cellular genes impacting human cytomegalovirus (HCMV) infection. It reveals JUNB as a key antiviral factor that the HCMV UL26 protein targets.
Area of Science:
- Virology
- Genetics
- Immunology
Background:
- CRISPR screening is vital for identifying genetic factors influencing viral infections.
- Existing methods for virus-focused CRISPR screens have limitations in identifying all relevant genes.
Purpose of the Study:
- To develop a scalable CRISPR screening pipeline, VIRCAA, for identifying cellular determinants of human cytomegalovirus (HCMV) infection.
- To investigate the role of the HCMV UL26 protein in viral infection and host-pathogen interactions.
Main Methods:
- Development of the VIRCAA (virally induced remodeling of cellular antibody affinity) screening pipeline.
- Application of the pipeline to analyze proteomic and transcriptomic data related to HCMV UL26.
- Investigating the interaction between HCMV UL26 and the cellular factor JUNB.
Main Results:
- The VIRCAA pipeline successfully identified cellular genes impacting HCMV infection across different life cycle stages.
- JUNB was identified as a crucial factor that drives antiviral gene expression and protein ISGylation, suppressing various viral infections.
- HCMV UL26 was found to interact with JUNB and inhibit its function in viral DNA replication compartments.
Conclusions:
- The VIRCAA pipeline is a powerful and scalable tool for discovering cellular determinants of viral infections.
- JUNB plays a significant role in antiviral defense, and HCMV has evolved mechanisms to counteract it via UL26.
- Understanding these interactions provides insights into host-pathogen dynamics and potential therapeutic targets.
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