Of four groups of chickens, two (groups I and II) were infected with MDV and two were not (groups III and IV). Groups I and III were fed diets low in lipid, and groups II and IV were fed cholesterol-supplemented diets. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of infected normocholesterolemic and hypercholesterolemic chickens (groups I and II). In contrast, grossly visible atherosclerotic lesions were not seen in uninfected normocholesterolemic chickens (group III), nor in uninfected hypercholesterolemic chickens (group IV). Microscopically, arterial changes in the infected animals were characterized by occlusive fibromuscular intimal thickening which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in man. These results may have important bearing on our understanding of the etiology and pathogenesis of human arteriosclerosis since there is widespread and persistent infection of human populations with up to five different herpes-viruses.

SUMMARYThe RB-1B and ALA-8 strains of Marek's disease (MD) virus, which were isolated from chickens with MD and which had been vaccinated with the herpesvirus of turkeys (HVT), were evaluated for their oncogenic potential in genetically susceptible (P-line) and resistant (N-line, PDRC) chickens. RB-1B and ALA-8 were both highly oncogenic, causing a high incidence of MD in both susceptible and resistant birds. Vaccination of P-line birds with SB-1 or HVT did not protect satisfactorily against RB-1B. However, a bivalent vaccine consisting of SB-1 and HVT enhanced protection significantly. HVT alone, and the bivalent vaccine, protected PDRC and N-line chickens well against RB-1B, but SB-1 was less protective in PDRC birds. HVT protected equally well against challenge with ALA-8 and the standard JM-10 strain. Differences in the pathogenesis of viral infection could not be detected among ALA-8, RB-1B and JM-10 between 4-7 days postinfection (d.p.i.). However, after d.p.i. 12 RB-1B caused significantly higher levels of viral internal antigen and virus isolation rates than did JM-10 in the same genetic strain. Prior vaccination prevented the expression of ALA-8 at 5 and 20 d.p.i., but not that of RB-1B. Pathogenetic events such as expression of VIA or level of virus infection appeared to be directly related to the level of protection observed in challenged birds.

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