|Niikura, Masahiro - MICHIGAN STATE UNIVERSITY|
|Dodgson, Jerry - MICHIGAN STATE UNIVERSITY|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: March 1, 2006
Publication Date: March 1, 2006
Citation: Niikura, M., Dodgson, J., Cheng, H.H. 2006. Direct evidence of host genome acquisition by the alphaherpesvirus Marek's disease virus (MDV)[Abstract]. Keystone Symposia: Cell Biology of Virus Entry, Replication and Pathogenesis. p. 69 Technical Abstract: Many herpesviruses including MDV, a poultry alphaherpesvirus, carry homologous host genes presumably acquired during viral evolution. We have characterized one recent acquisition by MDV. The virulent MDV strain Md11 was isolated from a commercial chicken and propagated initially on duck cells. In the process of cloning the entire Md11 genome in a bacterial artificial chromosome (BAC) vector, we obtained an infectious clone in which the entire terminal repeat short segment (TRS) was replaced by a portion of the duck genome. The acquired 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. MDV generated from this infectious MDV-BAC clone can induce lymphomas in infected birds, the major hallmark of Marek’s disease, however, at a frequency considerably lower than the parental Md11 virus stock. We are currently investigating whether the replacement of the TRS with host genome DNA influences tumor incidence. 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 strictly cell-associated nature of its infection process.