The influence of the major histocompatibility locus on Marek's disease in the chicken.

Abstract

In the early to mid 1960’s Marek’s disease was becoming a severe problem to the poultry industry. This served as a stimulus for our laboratory to initiate research on the disease which eventually evolved to a concerted effort in the late 1960Ts and early 1970Ts. Early studies were plagued by an inability to obtain reproducible results from trial to trial. However, a report by Sevoian (1962) established reliable methodology and facilitated the development of long range research programs. In a relatively short period of time, tissue culture propagation was documented (Churchill and Biggs, 1967; and Solomon, et al., 1968), the causative agent, a DNA virus was found (Biggs, et al., 1968; and Nazerian et al., 1968), its infectious characteristics were intensely investigated (Witter, et al., 1969; Purchase and Biggs, 1967; and Biggs, 1968), and a protective vaccine was developed (Churchill, et al., 1969; and Okazaki et al., 1970). Concurrently, genetic studies were being made by a number of investigators throughout the world. A great amount of effort on the genetic control of Marek’s disease was made by the Northeastern (NE-60) Regional Cooperative Breeding project of which the Regional Poultry Research Laboratory was a member. The general consensus of opinion was that genetic differences in susceptibility existed in both meat and egg type chickens, but it was a difficult task to markedly alter the susceptibility state. Fortunately, lines did exist at East Lansing (Table 1) as well as other locations which showed extreme differences in Marek’s disease susceptibility and lent themselves favorably to the study of genetic control mechanisms.