SUMMARY. Marek’s disease (MD) is an oncogenic, lymphoproliferative and highly-contagious disease of chickens. Its etiologic agent is the alphaherpesvirus Marek’s disease virus (MDV, Gallid alphaherpesvirus 2 ), and it is a chronic and ubiquitous problem for the poultry industry with significant economic impact in the United States and worldwide. We have previously demonstrated that MDV attenuated by dicodon pair deoptimization of the U L 54 gene results in reduced gene product accumulation in vitro , with reduced viral genome copy number upon infection and reduced atrophy of bursa and thymus in vivo as well. In this report we detail our attempts to use the same attenuation strategy on a meq -deleted MDV mutant, rMd5B40∆Meq. Unlike the wild type rMd5B40 virus the rMd5B40∆Meq is no longer oncogenic, but infected birds experience an unacceptable amount of bursa and thymus atrophy (BTA). We produced two meq -deleted MDV recombinants with a dicodon deoptimized U L 54 (rMd5B40∆Meq/U L 54deop1 and -2) and tested their ability to cause BTA and to serve as a protective vaccine. We found that, while dicodon deoptimization of the U L 54 gene results in a virus which spares the infected animal from atrophy of the bursa and thymus, the meq -deleted, U L 54-deoptimized recombinant rMd5B40∆Meq/U L 54deop2 is also less protective than the meq -deleted virus without U L 54 deoptimization, the HVT + SB1 combination vaccine, or the Rispens (CVI988) vaccine.

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