Contrasting Characteristics of Marek’s Disease Herpesvirus Isolated from Chickens with and without Avian Leukosis Virus Infection

Abstract

Marek’s disease herpesvirus (MDHV) isolated from chickens free of naturally occurring avian leukosis virus (ALV) infection produced characteristic foci in both chicken embryo fibroblast (CEF) and chicken kidney cell (CKC) cultures. MDHV-A, which was extracted from the feather follicle epithelium of chickens naturally infected with ALV, did not induce cy tologic changes in CEF cultures, but did cause focus formation in CKC cultures. ALV was detected in MDHV-A, but not in MDHV preparations. MDHV-A (reconstructed in vivo) and MDHV were further distinguished from one another by inoculation of ALV-free LSI-SPF chickens. MDHV-A elicited a high incidence of early mortality which was not accompanied by the gross tumor spectrum characteristic of Marek’s disease, although extensive histologic lesions were present. The differences between MDHV and MDHV-A were not as striking in another line of ALV-free chickens (SPAFAS). By contrast, among conventional chickens with naturally occurring ALV infection, neither MDHV-A nor MDHV caused appreciable early mortality although both were highly oncogenic (gross tumor development). These observations demonstrate that the presence of an oncornavirus (ALV), detected by radioimmune but not complement fixation assays, can influence the in vitro and in vivo characteristics of an oncogenic herpesvirus (MDHV). The observations recorded here resolve some of the inconsistencies reported in the literature. Thus, the apparent failure by some to find interactions between MDHV and oncornaviruses can be ascribed to the comparatively limited sensitivity of the complement fixation assay used to detect oncornaviruses (ALV). We have shown that the presence of oncornavirus detectable by radioimmune assay, but not by complement fixation, can influence the in vitro and in vivo responses of an oncogenic herpesvirus (MDHV). Our observations relating to viral interaction do not imply that MDHV required the presence of ALV to produce disease.