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Published on: July 29, 2014
The Role of RNA Sensors in Regulating Innate Immunity to Gammaherpesviral Infections
Huirong Zhang1, Praneet K Sandhu1, Blossom Damania1
1Department of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Abstract:
Kaposi's sarcoma-associated herpesvirus (KSHV) and the Epstein-Barr virus (EBV) are double-stranded DNA oncogenic gammaherpesviruses. These two viruses are associated with multiple human malignancies, including both B and T cell lymphomas, as well as epithelial- and endothelial-derived cancers. KSHV and EBV establish a life-long latent infection in the human host with intermittent periods of lytic replication. Infection with these viruses induce the expression of both viral and host RNA transcripts and activates several RNA sensors including RIG-I-like receptors (RLRs), Toll-like receptors (TLRs), protein kinase R (PKR) and adenosine deaminases acting on RNA (ADAR1). Activation of these RNA sensors induces the innate immune response to antagonize the virus. To counteract this, KSHV and EBV utilize both viral and cellular proteins to block the innate immune pathways and facilitate their own infection. In this review, we summarize how gammaherpesviral infections activate RNA sensors and induce their downstream signaling cascade, as well as how these viruses evade the antiviral signaling pathways to successfully establish latent infection and undergo lytic reactivation.
Insights
Kaposi
Area of Science:
- Virology and Immunology
- Oncology
Background:
- Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) are oncogenic gammaherpesviruses linked to human cancers.
- These viruses establish lifelong latent infections with periods of lytic replication.
- Viral and host RNA transcripts activate innate immune sensors like RLRs, TLRs, PKR, and ADAR1.
Purpose of the Study:
- To review how gammaherpesviruses activate RNA sensors and downstream signaling.
- To summarize viral evasion strategies against antiviral signaling pathways.
- To understand how these viruses establish latency and reactivate.
Main Methods:
- Review of existing literature on KSHV and EBV infection.
- Analysis of viral and host interactions with RNA sensors.
- Examination of immune evasion mechanisms employed by gammaherpesviruses.
Main Results:
- Gammaherpesviral infections trigger innate immune responses via RNA sensor activation.
- KSHV and EBV employ viral and cellular factors to inhibit these antiviral pathways.
- Successful immune evasion is crucial for viral latency and reactivation.
Conclusions:
- Understanding RNA sensor activation and viral evasion is key to combating KSHV/EBV-associated malignancies.
- Targeting these pathways may offer novel therapeutic strategies against gammaherpesvirus infections.
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