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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Endemic Poultry Viral Diseases Research » Research » Publications at this Location » Publication #370703

Research Project: Genetic and Biological Determinants of Avian Herpesviruses Pathogenicity, Transmission, and Evolution to Inform the Development of Effective Control Strategies

Location: Endemic Poultry Viral Diseases Research

Title: The Secretion of Type I Interferons as a Primary Determinant of Susceptibility to Marek’s Disease Virus in Chickens

item Conrad, Steven
item Hearn, Cari
item Dunn, John

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/14/2020
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Marek’s disease (MD) is a highly-contagious lymphoproliferative disease of chickens. In addition to neuroinflammation and profound immunosuppression, afflicted chickens develop visceral tumors derived from transformed CD4+ T cells. Its etiologic agent is Marek’s disease virus (MDV), an alphaherpesvirus of the subfamily Alphaherpesvirinae, genus Mardivirus. Because it is ubiquitous in the environment, MDV is controlled by universal vaccination with live-attenuated viruses such as the Rispens (CVI988) strain of MDV, or with the heterologous virus Turkey herpesvirus (HVT). For over 50 years susceptibility and resistance to MD has been studied using chicken lines selected for their propensity to develop tumors upon infection with MDV and subsequently inbred to reduce genetic variation. The lines 63 (resistant) and 72 (susceptible) are two such inbred lines. These two lines are congenic for the MHC haplotype B*2 and therefore eliminate consideration of MHC as a factor in determining susceptibility or resistance to MD pathology. In the macrophage-like cell HD11 and in primary macrophages isolated from 63 and 72 animals we have demonstrated that simulated infection elicits different amounts of the type I interferons (IFNs) IFNA and IFNW1, with the susceptible line 72 producing only a weak pulse of the type I IFNs. We hypothesize that this difference in the amount of type I IFN produced, and the concomitant reduction in production of the interferon-stimulated genes (ISGs), is a major driver of resistance and susceptibility in these two chicken lines.