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Updated: Jul 19, 2026

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
Published on: September 14, 2010
Kaposi sarcoma herpesvirus-encoded interferon regulator factors
1Winship Cancer Institute, 1365-B Clifton Rd NE, Atlanta, GA 30322, USA. mofferm@emory.edu
Abstract:
The Kaposi sarcoma herpesvirus (KSHV) encodes multiple proteins that disrupt host antiviral responses, including four viral proteins that have homology to the interferon regulatory factor (IRF) family of transcription factors. At least three of the KSHV vIRFs (vIRFs 1-3) alter responses to cellular IRFs and to interferons (IFNs), whereas functional changes resulting from the fourth vIRF (vIRF-4) have not been reported. The vIRFs also affect other important regulatory proteins in the cell, including responses to transforming growth factor beta (TGF-beta) and the tumor suppressor protein p53. This review examines the expression of the vIRFs during the life cycle of KSHV and the functional consequences of their expression.
Insights
Kaposi sarcoma herpesvirus (KSHV) viral interferon regulatory factors (vIRFs) disrupt host antiviral defenses. This review explores vIRF expression and function, impacting cellular IRFs, interferons, TGF-beta, and p53.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Kaposi sarcoma herpesvirus (KSHV) encodes viral proteins that interfere with host antiviral mechanisms.
- Four KSHV-encoded proteins (vIRFs) are homologous to host interferon regulatory factors (IRFs).
Purpose of the Study:
- To review the expression patterns of KSHV vIRFs throughout the viral life cycle.
- To elucidate the functional consequences of vIRF expression on host antiviral responses and cellular pathways.
Main Methods:
- Literature review of studies on KSHV vIRFs.
- Analysis of reported data on vIRF interactions with host factors.
Main Results:
- KSHV vIRFs (vIRF1-3) modulate cellular IRFs and interferon (IFN) signaling.
- vIRFs also impact transforming growth factor beta (TGF-beta) and p53 pathways.
- The specific functions of vIRF-4 remain largely uncharacterized.
Conclusions:
- KSHV vIRFs are critical viral effectors that subvert host immunity and cellular regulation.
- Understanding vIRF functions is essential for comprehending KSHV pathogenesis and developing therapeutic strategies.
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