Histocompatibility of chicken populations selected for resistance to Marek's disease

Pazderka, F.; Longenecker, B. M.; Law, G. R. J.; Stone, Howard A.; Ruth, R. F.

doi:10.1007/bf01572279

Cited by 102 publications

(32 citation statements)

References 7 publications

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“…Genetics play a crucial role in disease outcome, and as such MHC has been shown to be a major contributor (3). However, despite s t r o n g c o n t r i b u t i o n of the MHC haplotype, other genes also contribute to resistance, as exemplified by line 6 and 7 strains that share the B 2 locus (40). The susceptible line 7 chickens develop clinical MD, and h a ve been shown to amplify t h e virus to a much higher level (6,12).…”

Section: Introductionmentioning

confidence: 99%

Early Replication in Pulmonary B Cells After Infection with Marek's Disease Herpesvirus by the Respiratory Route

Baaten¹,

Staines²,

Smith³

et al. 2009

Viral Immunology

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Natural infection with Marek's disease virus occurs through the respiratory mucosa after chickens inhale dander shed f r o m i n fected c h i c k e n s . The early events in the lung following exposure to the feather and squamous epithelial cell debris containing the viral particles remain unclear. In order to elucidate the virological and immunological consequences of MDV infection for the respiratory tract, chickens were infected by intratracheal administration of infective dander. Differences between susceptible and resistant chickens were immediately apparent, with delayed viral replication and earlier onset of interferon (IFN)-g production in the latter. CD4 þ and CD8 þ T cells surrounded infected cells in the lung. Although viral replication was evident in macrophages, pulmonary B cells were the main target cell type in susceptible chickens following i n t r a t r a c h e a l infection with MDV. In accordance, depletion of B cells curtailed viremia and substantially affected pathogenesis in susceptible chickens. Together the data described here demonstrate the role of pulmonary B cells as the primary and predominant target cells and their importance for MDV pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Early Replication in Pulmonary B Cells After Infection with Marek's Disease Herpesvirus by the Respiratory Route

Baaten¹,

Staines²,

Smith³

et al. 2009

Viral Immunology

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show abstract

“…Despite this, other genes also have a strong influence on MD resistance. This has been determined predominantly in studies of the MHC-congenic lines 6 1 (resistant) and 7 2 (susceptible), which were developed in East Lansing, MI, which differ in their resistance to a large number of MDV isolates (38). Several potential MD resistance quantitative trait loci (QTL) have been identified from crosses between these lines and others (48,52,33,11,19), but relatively few actual genes have been associated with the disease.…”

mentioning

confidence: 99%

Systems Analysis of Immune Responses in Marek's Disease Virus-Infected Chickens Identifies a Gene Involved in Susceptibility and Highlights a Possible Novel Pathogenicity Mechanism

Smith

Sadeyen

Paton

et al. 2011

J Virol

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Marek's disease virus (MDV) is a highly contagious oncogenic alphaherpesvirus that causes disease that is both a cancer model and a continuing threat to the world's poultry industry. This comprehensive gene expression study analyzes the host response to infection in both resistant and susceptible lines of chickens and inherent expression differences between the two lines following the infection of the host. A novel pathogenicity mechanism, involving the downregulation of genes containing HIC1 transcription factor binding sites as early as 4 days postinfection, was suggested from this analysis. HIC1 drives antitumor mechanisms, suggesting that MDV infection switches off genes involved in antitumor regulation several days before the expression of the MDV oncogene meq. The comparison of the gene expression data to previous QTL data identified several genes as candidates for involvement in resistance to MD. One of these genes, IRG1, was confirmed by single nucleotide polymorphism analysis to be involved in susceptibility. Its precise mechanism remains to be elucidated, although the analysis of gene expression data suggests it has a role in apoptosis. Understanding which genes are involved in susceptibility/resistance to MD and defining the pathological mechanisms of the disease gives us a much greater ability to try to reduce the incidence of this virus, which is costly to the poultry industry in terms of both animal welfare and economics.

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“…Well-characterised correlations between MHC class I alleles and disease resistance are described for Marek's disease in chickens [5,6], and malaria [7] and HIV [8] in humans.…”

mentioning

confidence: 99%

Differences in MHC class I genes between strains of rainbow trout ( )

Xia

Kiryu

Dijkstra

et al. 2002

Fish & Shellfish Immunology

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Histocompatibility of chicken populations selected for resistance to Marek's disease

Cited by 102 publications

References 7 publications

Early Replication in Pulmonary B Cells After Infection with Marek's Disease Herpesvirus by the Respiratory Route

Early Replication in Pulmonary B Cells After Infection with Marek's Disease Herpesvirus by the Respiratory Route

Systems Analysis of Immune Responses in Marek's Disease Virus-Infected Chickens Identifies a Gene Involved in Susceptibility and Highlights a Possible Novel Pathogenicity Mechanism

Differences in MHC class I genes between strains of rainbow trout ( )

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