Page Banner

United States Department of Agriculture

Agricultural Research Service

Research Project: EMPLOYING GENOMICS, EPIGENETICS, AND IMMUNOGENETICS TO CONTROL DISEASES INDUCED BY AVIAN TUMOR VIRUSES

Location: Avian Disease and Oncology Laboratory

Title: Characterizing a point mutation within the UL5 gene that reduces in vivo replication and MD incidence

Authors
item Hildebrandt, Evin -
item Dunn, John
item Cheng, Hans

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: July 20, 2014
Publication Date: July 20, 2014
Citation: Hildebrandt, E., Dunn, J.R., Cheng, H.H. 2014. Characterizing a point mutation within the UL5 gene that reduces in vivo replication and MD incidence [abstract]. In: Proceeding for 10th International Symposium on Marek's Disease and Avian Herpesviruses, July 20-23, 2014, East Lansing, Michigan. p. 58.

Technical Abstract: Marek’s disease virus (MDV) is an oncogenic alphaherpesvirus of chickens and the causative agent for Marek’s disease (MD). Vaccination is the primary method to control MD. Despite the success of vaccination, more virulent field strains are evolving, requiring the development of new vaccines. Attenuation via in vitro serial passage has successfully generated several MD vaccines, yet better understanding of the genes involved in attenuation should assist in future vaccine development. Serial passage and sequencing of three MDV replicates identified candidate mutations involved in attenuation including a single point mutation within the UL5 helicase-primase subunit gene. This mutation significantly decreased in vivo replication and virulence of the virus, causing in a reduction of MD incidence by nearly 90%. To further characterize this point mutation, the protective index of the UL5 mutant as a candidate vaccine was compared to commercial HVT and Bivalent vaccines. We found the UL5 recombinant virus did provide protection against challenge with virulent MDV. Additional trials with UL5 in combination with other mutations, such as deletion of the Meq oncogene, are currently underway. Our objective is to determine if incorporation of the UL5 mutation eliminates bursal-thymus atrophy, which is a characteristic of the 'Meq virus, by reducing in vivo replication of the virus. Vaccinal protection of the UL5+'Meq double mutant will also be compared to the original 'Meq virus and commercial Bivalent and Rispens vaccines. Cumulatively, our efforts should assist in the rationale design of future MD vaccines.

Last Modified: 9/21/2014
Footer Content Back to Top of Page