Studies on Acute Marek's Disease IV. Relative Susceptibility of Different Lines and Crosses of Chickens to GA Isolate

Schmittle, S. C.; Eidson, C. S.

doi:10.2307/1588440

Cited by 11 publications

(4 citation statements)

References 7 publications

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“…7C and D , is caused by a virus t h a t is mainly s p r e a d by contact e x p o s u r e . The ability to infect chickens via the respiratory tract has been demonstrated by studies performed as early as the 1970s; infection through contact exposure with airborne suspensions of infective dander (1,9,15,31,32) and with infected individuals (34,39,48), administration of feather tip extracts (16,21), as well as cell-associated virus (38) were all shown to cause MD. However, some characteristics of these approaches, such as reproducibility issues, inability to deliver a quantifiable dose of virus, The effect of intratracheal infection on macrophages in the lung was assessed by immunohistology.…”

Section: Pulmonary B Cells Are Primarily Infected Following MDV Infecmentioning

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: Pulmonary B Cells Are Primarily Infected Following MDV Infecmentioning

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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“…The first investigators (Waters, 1945;Heisdorf et al, 1947) found no relationship between the two methods; later, others (Biggs et al, 1968;Schmittle and Eidson, 1968;Grunder et al, 1972) found a positive correlation. These conflicting results may have been due to confusion between visceral MD lymphomas and lymphoid leukosis, both of which were termed "lymphomatosis" by early investigators.…”

Section: Discussionmentioning

confidence: 97%

“…Since 1966, it has been reported that, some strains of fowls are more resistant to MD than others and in many of these studies males were found to be more resistant than females (Biggs et al, 1968;Cole, 1968;Schmittle and Eidson, 1968;Morris et al, 1970;Grunder etal, 1972 andMorrisroe, 1970 and1976).…”

Section: Discussionmentioning

confidence: 99%

The development of two white Plymouth Rock lines resistant to Marek's disease by breeding from survivors¹

et al. 1981

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SUMMARYA programme to develop resistance to Marek's disease (MD) in chickens in two non-inbred White Plymouth Rock (WPR) lines by breeding from survivors was initiated in 1968 and since then nine generations have been produced. In each generation only sires and dams which survived heavy exposure to virulent MD virus (MDV), Dutch strain K, either by inoculation (for the first two generations) or by contact-exposure (for the following seven generations) were used.In this long term trial a high level of resistance to MD was reached within five generations; thereafter no marked further increase in resistance could be obtained. Susceptibility to MD, reflected by MD mortality in each generation, was expressed as % incidence of MD.Statistical evaluation of MD susceptibility in the nine generations of the two lines revealed a significant interaction between MD mortality and two sources of variation, sex and generation. No overall line effect was found, but there was a significant line x generation interaction. The remaining interactions were not significant. Results indicate that breeding from survivors for development of resistance to MD is feasible. Exposure of birds to either artificial (by injection) or

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“…The methods used to measure resistance to Marek's disease were natural exposure (Waters, 1945;Hutt and Cole, 1947;Bearse et al, 1963), or injection with MDVcontaining blood or tumour cells (Biggs et al, 1968;Cole, 1968;Schmittle and Eidson, 1968;Hartmann and Sanz, 1971;Grander et al, 1972). Birds from different genetic stock exposed to MDV either naturally or artificially show no differences in ranking of their MD incidence.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of resistance to Marek's disease in three white Plymouth rock unes and in two reciprocal crosses

Jh³

et al. 1982

Avian Pathology

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SUMMARYTwo White Plymouth Rock lines (WPR), both developed into lines resistant for Marek's disease (MD), and one commercial WPR line, supposedly susceptible to the disease, were mated in a number of combinations to evaluate resistance to MD in their pure-and crossbred progeny. For this purpose the pedigreed 1-day-old progeny chicks were exposed to 3-week-old spreader chicks which had been inoculated at 1-day-old with virulent MD virus (MDV) and reared with them for the whole experimental period of 15 weeks.Response to the challenge showed that resistance to MD in the crossbreds was intermediate to that of resistant and susceptible parental Unes. It appeared that, besides a sex effect in the male progeny, the trait for MD resistance was most effectively transferred to the crossbred progeny by the resistant male parents.

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Studies on Acute Marek's Disease IV. Relative Susceptibility of Different Lines and Crosses of Chickens to GA Isolate

Cited by 11 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

The development of two white Plymouth Rock lines resistant to Marek's disease by breeding from survivors¹

Evaluation of resistance to Marek's disease in three white Plymouth rock unes and in two reciprocal crosses

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Studies on Acute Marek's Disease IV. Relative Susceptibility of Different Lines and Crosses of Chickens to GA Isolate

Cited by 11 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

The development of two white Plymouth Rock lines resistant to Marek's disease by breeding from survivors1

Evaluation of resistance to Marek's disease in three white Plymouth rock unes and in two reciprocal crosses

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The development of two white Plymouth Rock lines resistant to Marek's disease by breeding from survivors¹