Skip to main content
ARS Home » Research » Publications at this Location » Publication #188614
Title: ONCOGENIC MAREK'S DISEASE VIRUSES LACKING THE 132 BASE PAIR REPEATS CAN STILL BE ATTENUATED BY SERIAL IN VITRO CELL CULTURE PASSAGES

Author
item Silva, Robert
item Gimeno, Isabel

Submitted to: Virus Genes
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/18/2006
Publication Date: 12/31/2006
Citation: Silva, R.F., Gimeno, I.M. 2006. Oncogenic Marek's disease viruses lacking the 132 base pair repeats can still be attenuated by serial in vitro cell culture passages. Virus Genes. 34(1):87-90.

Interpretive Summary: Marek’s disease is an important disease of poultry and is caused by Marek’s disease virus (MDV). The most effective vaccines for Marek’s disease are made by attenuating MDV by serially passing the virus in tissue culture cells. How passing the virus in cell culture results in attenuation is not known. However, in every case when the virus is passed in cell culture, a region of the MDV genome increases in size. It has long been believed that this increase in size is the reason the virus becomes attenuated. We made mutations in the MDV genome and demonstrated that the observed increase in size is not responsible for attenuation. Our finding indicates that trying to use molecular biology to alter or mutate this region of the MDV genome will not result in generating any potentially useful new vaccines.

Technical Abstract: Marek’s disease virus (MDV) can be attenuated by serially passing the virus in cell culture. During cell culture passage, two copies of a 132 bp repeat are expanded to over 30 copies. We deleted the two copies of the 132 bp repeat region in a pathogenic MDV and demonstrated that the virus was still pathogenic. The pattern and frequency of tumors in the parental and mutant virus were the same. Early virus replication, and the appearance of persistent neurological lesions were also similar between the parental and deleted virus. Nevertheless, wild-type MDV and the deletion virus could be attenuated by serial in vitro cell culture passages. Based upon analyzing the passage 40 viruses, attenuation of the MDV lacking the 132 bp repeats appears to occur in a manner that is analogous to the process occurring wild-type MDV attenuation. Whatever process is involved in the cell-culture attenuation of MDV, the mechanism does not involve the 132 bp repeat region.