Format

Send to

Choose Destination
Virology. 2014 Jan 5;448:55-64. doi: 10.1016/j.virol.2013.09.017. Epub 2013 Oct 20.

Virus-encoded miR-155 ortholog is an important potential regulator but not essential for the development of lymphomas induced by very virulent Marek's disease virus.

Author information

1
Key Laboratory of Animal Immunology of the Ministry of Agriculture, Henan Provincial Key Laboratory of Animal Immunology, Henan Academy of Agricultural Sciences, No.116 Huayuan Road, Zhengzhou 450002, People's Republic of China; College of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, People's Republic of China; College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471003, People's Republic of China.

Abstract

The microRNA (miRNA) mdv1-miR-M4, a functional miR-155 ortholog encoded by oncogenic Marek's disease virus (MDV), has previously been suggested to be involved in MDV pathogenesis. Using the technique of bacterial artificial chromosome mutagenesis, we have presently evaluated the potential role of mdv1-miR-M4 in the oncogenesis of the very virulent (vv) MDV strain GX0101. Unexpectedly, deletions of the Meq-cluster or mdv1-miR-M4 alone from the viral genome strongly decreased rather than abolished its oncogenicity. Compared to GX0101, mortalities of mutants GXΔmiR-M4 and GXΔMeq-miRs were reduced from 100% to 18% and 4%, coupled with the gross tumor incidence reduction from 28% to 22% and 8%, respectively. Our data suggests that the mdv1-miR-M4 is possibly an important regulator in the development of Marek's disease (MD) lymphomas but is not essential for the oncogenicity of vvMDV. In addition, some of the other Meq-clustered miRNAs may also play potentially critical roles in vvMDV induction of lymphomas.

KEYWORDS:

BAC; MDV; MicroRNA; Oncogenesis; Pathogenesis; mdv1-miR-M4; miR-155

PMID:
24314636
DOI:
10.1016/j.virol.2013.09.017
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center