Titlebook: Marek’s Disease; Kanji Hirai Book 2001 The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer-Verlag GmbH, D

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Kanji HiraiIncludes supplementary material:

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,Pathogenesis of Marek’s Disease Virus Infection,a specific pathologic expression. However, other diseases are relatively complex in terms of pathogenesis; Marek’s disease (MD) most certainly belongs in this category. This chapter will concern itself with the spectrum of sequential events triggered by infection with MD virus (MDV), and the consequ

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,Protective Efficacy of Marek’s Disease Vaccines,ens against natural challenge with field strains of Marek’s disease (MD). This strategy has been unusually effective. In the United States, losses from the condemnation at slaughter of young broiler chickens with visible lesions of MD have decreased from 1.5% in 1970 to 0.0121% in 1999, a reduction

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,Immune Responses to Marek’s Disease Virus Infection,lated in 1968 and vaccines became available shortly afterwards (.,Witter 2000). The pathogenesis of MD has been reviewed extensively (.,.,.; .). Infection of chickens with MDV is characterized by several distinct phases in which innate and acquired immune responses play important roles. The first ph

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,The Genomic Structure of Marek’s Disease Virus,rs. In thin-section electron micrographs, an electron transparent region, termed the tegument, surrounds the capsid, which in turn is surrounded by a lipid-containing envelope. Variations in tegument thickness and the state of the envelope result in reports of enveloped herpesviruses varying from l2

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,Protein-Coding Content of the Sequence of Marek’s Disease Virus Serotype 1,on, based on its genomic organization and significant sequence similarity to other α-herpesviruses, such as herpes simplex virus (HSV) and varicella-zoster virus (VZV), it was classified in the subfamily . (.; .). Like other α-herpesviruses, MDV establishes a life-long latent infection, but differs