Over the last five decades, the pathogenicity of the Marek's disease virus (MDV) has evolved from the relatively mild strains (mMDV) observed in the 1960s to the more severe very-virulent-plus strains currently observed in today's outbreaks. The use of vaccines to control Marek's disease (MD), but not the infection cycle, is thought to be the major influence on the evolution of MDV. Selection for genetic resistance to MD has also been employed by the industry to control MD in the commercial setting but the role of host genetics on the evolution of MDV has been difficult to investigate in the field. To investigate the influence of vaccination and host resistance we developed a laboratory model to control and assess the effects of virus and animal genetics on MDV evolution. A bacterial artificial chromosome–derived MDV (Md5B40BAC) was used for in vivo passage (IVP) through turkey herpesvirus (HVT)-vaccinated resistant (MHC-B21) and susceptible (MHC-B13) genetic chicken lines. During IVP in the vaccinated susceptible line, the disease incidence increased from 23% MD in the first IVP to 53% MD during the fifth IVP. In the vaccinated resistant line, disease incidence increased from 0% MD during the first IVP to 29% MD during the fifth IVP. Although the IVP isolates remained relatively mild in the vaccinated resistant chicken line (29% MD) they increased from 0% to 63% MD when used to challenge the vaccinated susceptible chickens. There was no corresponding increase in disease incidence when the virus passed in the vaccinated susceptible genetic line was used to challenge the vaccinated resistant line. From this series of experiments we show that a cloned MDV (Md5B40BAC) can be selected by serial IVP to induce greater disease incidence in vaccinated chickens. This increase in disease incidence occurs in both susceptible and resistant chicken lines but is more easily observed in the susceptible line. Not surprisingly, both host genetics and vaccination play a role in selecting for increased MDV virulence. Our results suggest that the progressive increase in MDV virulence is partially masked as it circulates through vaccinated resistant genetic lines, but by applying this virus to less-resistant genetic lines, virus evolution can be clearly observed. We would predict that the introduction of more-resistant genetic lines into a commercial house contaminated with MDV circulating through susceptible lines would be less likely to produce vaccine breaks than placing susceptible lines into a house in which previously the MDV was circulating through resistant genetic lines.
La influencia del complejo mayor de histocompatibilidad y la vacunación con herpesvirus de los pavos sobre la evolución de la enfermedad del virus de Marek.
Durante las últimas cinco décadas, la patogenicidad del virus de la enfermedad de Marek (MDV) ha evolucionado desde las cepas relativamente leves (mMDV) observadas en la década de los 1960s, hasta las cepas más severas como las muy virulentas-plus (vv MDV) que actualmente se observan en los brotes actuales. Se cree que el uso de vacunas para el control de la enfermedad de Marek (MD) y no el ciclo de infección tiene la influencia mayor sobre la evolución del virus de Marek. La selección para la resistencia genética contra la enfermedad de Marek también ha sido empleada por la industria para controlar la enfermedad en el entorno comercial, pero ha sido difícil la investigación del papel de la genética del huésped en la evolución del virus de Marek en el campo. Para investigar la influencia de la vacunación y de la resistencia del hospedador, se desarrolló un modelo de laboratorio para controlar y evaluar los efectos de la genética de virus y animales sobre la evolución del virus de Marek. Se utilizó un virus de Marek derivado de un cromosoma bacteriano artificial (Md5B40BAC) para el pasaje en vivo (IVP) a través de líneas genéticas de pollos resistente
