|Niikura, Masahiro - MICHIGAN STATE UNIVERSITY|
|Dodgson, Jerry - MICHIGAN STATE UNIVERSITY|
Submitted to: Archives of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 3, 2005
Publication Date: December 31, 2006
Citation: Niikura, M., Dodgson, J., Cheng, H.H. 2006. Direct evidence of host genome acquisition by the alphaherpesvirus Marek's disease virus. Archives of Virology. 151:537-549. Available online. DOI 10.1007/S00705-005-0633-7. Interpretive Summary: Marek’s disease (MD) is an economically-important disease of chickens caused by a pathogenic virus known as the Marek’s disease virus (MDV). Currently, vaccines have controlled the problem but new emerging viral strains that vaccines cannot control are being encountered more frequently. The mechanism by which MDV strain becomes more virulent is not known. In this paper, we describe the identification of an MDV strain that incorporated a duck gene during its short time of maintenance outside of live chickens in laboratory-cultured duck cells. This result suggests that MDV and other viruses are able to “pirate” host genes, some of which may be advantageous to the virus. This information enhances our understanding of MDV evolution and suggests possibilities for improved control of MD.
Technical Abstract: Many herpesviruses including Marek's disease virus (MDV), a poultry alphaherpesvirus, carry homologous host genes presumably acquired during viral evolution. We have characterized one recent acquisition by MDV in considerable detail. The virulent MDV strain Md11 previously was isolated from a commercial chicken and initially propagated on duck cells. In the process of cloning the entire Md11 genome in a bacterial artificial chromosome (BAC), we obtained an infectious clone in which the entire terminal repeat short segment was replaced with a portion of the duck genome that corresponds to chicken chromosome 19. This sequence is not predicted to express any protein even though it contains one exon of the VAMP1 gene. The replacement did not affect MDV replication in vitro, despite the virus having only one copy of ICP4. Furthermore, we have shown that the variant MDV genome containing the duck genome substitution is present in the parental Md11 population and has been maintained through several subsequent propagations of the virus on chicken cells. This finding provides direct evidence that host genome acquisition by MDV actually occurs during virus replication, and that one or more such MDV genomes with host sequences may exist within MDV viral stocks which tend to be polyclonal, due to the cell-associated nature of its infection process.