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פותח על ידי קלירמאש פתרונות בע"מ -
The influence of ev6 on the immune response to avian leukosis virus infection in rapid-feathering progeny of slow- and rapid-feathering dams.
Year:
1991
Source of publication :
Poultry Science
Authors :
לוין, אילן
;
.
Volume :
70
Co-Authors:
Smith, E.J., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Fadly, A.M., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Levin, I., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Crittenden, L.B., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Facilitators :
From page:
1673
To page:
1678
(
Total pages:
6
)
Abstract:
Endogenous virus (EV) locus ev6 encodes only virus envelope glycoprotein. The influence of ev6 on the immune response to contact infection with hatchmates infected with avian leukosis virus (ALV) was compared in replicate hatches. The ALV Subgroup E-resistant, rapid-feathering (RF) female chickens produced by slow-feathering (SF) and RF dams with and without ev6 were exposed at hatch to hatchmates infected with ALV Subgroup A (Strain RPL-40). The RPL-40 viremia, shedding, and virus neutralizing antibodies were measured among pullets from two hatches at 22 wk of age. Although significant (P less than .05) differences between hatches in the immune response to contact infection were noted among ev6+ pullets, significantly fewer ev6+ pullets seroconverted than their ev6- hatchmates. At 22 wk of age, significantly more lymphomas were also found among ev6+ pullets than among ev6- hatchmates. In flocks wherein both parents and progeny were homozygous resistant to Subgroup E virus, there was no deterimental maternal effect on RF progeny from SF dams that carried ev21. These results also confirm that selection for genetic cellular resistance to Subgroup E ALV infection eliminates congenital transmission of EV21.
Note:
Related Files :
Animal
biosynthesis
Feathers
Female
Genetics
Growth, Development and Aging
Leukosis Virus, Avian
Male
עוד תגיות
תוכן קשור
More details
DOI :
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
20207
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:34
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Scientific Publication
The influence of ev6 on the immune response to avian leukosis virus infection in rapid-feathering progeny of slow- and rapid-feathering dams.
70
Smith, E.J., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Fadly, A.M., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Levin, I., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Crittenden, L.B., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
The influence of ev6 on the immune response to avian leukosis virus infection in rapid-feathering progeny of slow- and rapid-feathering dams.
Endogenous virus (EV) locus ev6 encodes only virus envelope glycoprotein. The influence of ev6 on the immune response to contact infection with hatchmates infected with avian leukosis virus (ALV) was compared in replicate hatches. The ALV Subgroup E-resistant, rapid-feathering (RF) female chickens produced by slow-feathering (SF) and RF dams with and without ev6 were exposed at hatch to hatchmates infected with ALV Subgroup A (Strain RPL-40). The RPL-40 viremia, shedding, and virus neutralizing antibodies were measured among pullets from two hatches at 22 wk of age. Although significant (P less than .05) differences between hatches in the immune response to contact infection were noted among ev6+ pullets, significantly fewer ev6+ pullets seroconverted than their ev6- hatchmates. At 22 wk of age, significantly more lymphomas were also found among ev6+ pullets than among ev6- hatchmates. In flocks wherein both parents and progeny were homozygous resistant to Subgroup E virus, there was no deterimental maternal effect on RF progeny from SF dams that carried ev21. These results also confirm that selection for genetic cellular resistance to Subgroup E ALV infection eliminates congenital transmission of EV21.
Scientific Publication
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