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Updated: Apr 16, 2026

Vaccinia Virus Infection & Temporal Analysis of Virus Gene Expression: Part 2
Published on: April 10, 2009
Caps off to poxviruses
1Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Abstract:
In this issue of Cell Host & Microbe, Liu et al. (2015) and Burgess and Mohr (2015) describe how two poxvirus mRNA decapping enzymes hijack a host 5'-to-3'-exoribonuclease to evade antiviral innate immunity by limiting accumulation of double-stranded RNA.
Insights
Two poxviruses possess mRNA decapping enzymes that hijack a host enzyme to evade antiviral immunity. This mechanism limits double-stranded RNA accumulation, a key trigger for innate immune responses.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Poxviruses are large DNA viruses that replicate in the cytoplasm.
- Antiviral innate immunity relies on detecting viral components, including double-stranded RNA (dsRNA).
- mRNA decapping is a crucial step in RNA metabolism, typically leading to RNA degradation.
Purpose of the Study:
- To investigate how poxviruses evade host antiviral immunity.
- To understand the role of poxviral mRNA decapping enzymes in this evasion.
- To elucidate the mechanism by which dsRNA accumulation is limited during poxvirus infection.
Main Methods:
- Analysis of poxvirus mRNA decapping enzyme function.
- Investigating interactions between viral and host cellular proteins.
- Assessing the impact of viral enzyme activity on host innate immune signaling pathways.
Main Results:
- Two distinct poxvirus mRNA decapping enzymes were identified.
- These viral enzymes were shown to interact with and hijack a host 5'-to-3'-exoribonuclease.
- This hijacking effectively limits the accumulation of dsRNA, thereby dampening the host antiviral response.
Conclusions:
- Poxviruses employ sophisticated strategies to subvert host antiviral defenses.
- Hijacking host RNA degradation machinery is a novel mechanism for immune evasion by viruses.
- Targeting host exoribonucleases allows poxviruses to control dsRNA levels and escape innate immunity.
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