Molecular mechanism of ORFV intervention strategies based on the UPS of host cell: a review.
- Author:
Yong-Zhong YU
1
;
Chun-Yu TONG
2
;
Bai-Fen SONG
2
;
Hong-Boi AN
2
;
Li-Yun YU
2
;
Li YU
3
;
Yu-Dong CUI
2
Author Information
1. College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing 163319, China. yyz1968@126.com
2. College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing 163319, China.
3. Division of Livestock Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150001, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Ecthyma, Contagious;
enzymology;
virology;
Host-Pathogen Interactions;
Humans;
Orf virus;
genetics;
physiology;
Proteasome Endopeptidase Complex;
metabolism;
Ubiquitin;
metabolism
- From:
Chinese Journal of Virology
2013;29(6):662-666
- CountryChina
- Language:Chinese
-
Abstract:
In order to compete the antiviral effects of the host cell in the process of infection, ORFV(known as Orf virus) relies on a series of functional genes developed through long-term population evolution, such as interferon resistance genes, Bcl-2 protein genes and cell cycle inhibitor gene and so on, with these weapons this virus is able to effectively counteract immune clearance and immune regulation from a host cell. Concurrently, ORFV also focuses on exploiting signal transduction pathways of the ubiquitin-proteasome system(UPS), circumvents the intracellular signal transduction and CD8+ T activation, for shielding virus particles towards maturation and releasing outside. This review introduced inner link between the UPS of host cell and intervention mechanism by virus, and analyzed the key roles of certains components in UPS, these all together showed the evolution tendency of ORFV that was involved in the designing of inhibition to immune response and for intracellular immune escape upon the selection pressure in host cell infected.
