Abstract

Marek's disease is an economically important disease of poultry and is caused by an alphaherpesvirus, Marek's disease virus (MDV). The predicted protein product of the MDV UL41 open reading frame has significant protein sequence identity with the virion host shutoff (vhs) protein gene in other alphaherpesviruses. To determine whether the MDV UL41 gene functions as a vhs protein, we utilized a transient co-transfection assay and demonstrated that the MDV UL41 protein was as active in degrading RNA as the vhs protein of herpes simplex virus type 1. To evaluate whether the MDV UL41 gene was involved in pathogenesis, we deleted the MDV UL41 gene. The UL41 deletion mutant replicated in cell culture as well as the parental MDV. The deletion mutant was inoculated into susceptible day-old chicks. The pattern and degree of tumor lesions and neurovirulence produced by the deletion mutant was same as the pattern of lesions induced by the parental virus. The only observable difference between the inoculation of MDV and the MDV deletion mutant was that the early in vivo cytolytic infection with the deletion mutant was of a longer duration than in the non-mutant MDV.

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