Abstract
Although the production of single gene knockout viruses is a useful strategy to study viral gene functions, the redundancy of many host interactive genes within a complex viral genome can obscure their collective functions. In this study, a rabbit-specific poxvirus, myxoma virus (MYXV), was genetically altered to disrupt multiple members of the poxviral ankyrin-repeat (ANK-R) protein superfamily, M-T5, M148, M149 and M150. A particularly robust activation of the NF-κB pathway was observed in A549 cells following infection with the complete ANK-R knockout (vMyx-ANKsKO). Also, an increased release of IL-6 was only observed upon infection with vMyx-ANKsKO. In virus-infected rabbit studies, vMyx-ANKsKO was the most extensively attenuated and produced the smallest primary lesion of all ANK-R mutant constructs. This study provides the first insights into the shared functions of the poxviral ANK-R protein superfamily in vitro and in vivo.
Original language | English (US) |
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Pages (from-to) | 134-145 |
Number of pages | 12 |
Journal | Virology |
Volume | 464-465 |
Issue number | 1 |
DOIs | |
State | Published - Sep 2014 |
Externally published | Yes |
Keywords
- Ankyrin-repeat
- Interleukin 6
- M-T5
- M148
- M149
- M150
- Myxoma virus
- Myxomatosis
- Nuclear factor kappa B
- Poxvirus
ASJC Scopus subject areas
- Virology