Abstract
Genetic resistance to avian tumor virus-induced tumorigenesis and vaccine protective efficacy preventing such tumorigenicity are determined by multiple factors including host genetics, viral virulence, dose of challenge viruses, type of vaccine, vaccine dosage, and interval between vaccination and viral exposure time. Studies on human immune response to vaccination suggest host genetic variability has a strong effect and involves both genes within and outside of the major histocompatibility complex (MHC). Using chickens primarily from two highly inbred and specific pathogen free lines (63 and 72) sharing a common MHC (B*2) haplotype in challenge trials, we recently reported a striking difference in protective efficacy conveyed by HVT or CVI988/Rispens at either 500 PFU/bird or a commercial dosage. We also reported DNA methylation level that differs between the two lines of chickens at promoter regions of genes. Differential gene expression was also reported. This report documents Marek’s disease (MD) incidences of the two highly inbred lines and a series of Recombinant Congenic Strains (RCS) derived from the two lines, which were induced with a very virulent plus strain of MD virus, and illustrates genetic and epigenetic differences between the lines, which we anticipate, at least in part, are liable to the observed MD incidence and vaccine efficacy differences. The genetic and epigenetic mechanisms underlying both genetic resistances to MD and vaccine protective efficacy are complex. Therefore, continuous and systematic efforts on such study are warranted. A better understanding on genetic resistance to MD will empower the disease control through genetic or genomic selection, and a better understanding on the roles of host genetics in relation to immunogenicity in response to vaccination will serve as the touchstone for rational design and development of safer and more efficacious vaccines against infectious diseases.
Highlights
Marek’s disease (MD) is a α-herpesvirus-induced T-cell lymphoma in chickens [1,2]
MD incidences for the Recombinant Congenic Strains (RCS) ranked from 0% up to 41% (RCS-M; Figure 2)
We recently showed non-major histocompatibility complex (MHC) genetic variation, in addition to MHC B haplotype that was primarily reported by Bacon and Witter in the 1990s [2326,57], plays an important role in modulating MD vaccine efficacy [31,32,33]
Summary
Marek’s disease (MD) is a α-herpesvirus-induced T-cell lymphoma in chickens [1,2]. MD historically caused devastating losses to the poultry industry worldwide but has been under control since the 1970s by wide use of vaccination [3,4,5,6]. Our data clearly showed genes outside of the MHC region significantly affect MD vaccine protective efficacy. Our data showed for the first time there may be a chicken line by vaccine interaction modulating MD vaccine protective efficacy. Based on the above findings our long-term goal is to determine what are the genetic and epigenetic differences between the genetic lines of chickens that modulate the differential protective efficacy of MD vaccines against vv+ MDV challenge when the other factors listed above are similar or identical. Data from our recent collaborative studies showed that profiles of global gene expression with or without MDV challenge differ between the highly inbred line 63 and 72 and one recombinant congenic strain [36]. Our data provided additional experimental evidence in elucidating genetic and epigenetic factors that may modulate MD genetic resistance to MD and the differential immune response to MD vaccine between the genetic lines of chickens
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