SummaryAnimal production efficiency, and product volume and quality can be greatly increased by reducing disease losses. Genetic variation, a prerequisite for successful selection, has been found in animals and poultry exposed to a variety of viral, bacterial and parasitic infections. Breeding for disease resistance can play a significant role alone or in combination with other control measures including disease eradication, vaccination and medication.Feasibility of simultaneously improving resistance to specific diseases and production traits has been demonstrated. However, selection for specific resistance to all diseases of animals and poultry is impossible. Development of general disease resistance through indirect selection primarily on immune response traits may be the best long‐term strategy but its applicability is presently limited by insufficient understanding of resistance mechanisms. Another hindrance may be negative genetic correlations among various immune response functions: phagocytosis, cell mediated and humoral immunity. To better assess the feasibility of increasing general disease resistance by indirect selection we must obtain estimates of heritability for immune response, disease resistance, and economic production traits, as well as genetic correlations among these traits.The present level of disease resistance in farm animals resulted from natural selection and from correlated responses to selection for production traits while the influence of artificial selection for resistance was minimal. Future research should be directed towards developing and applying breeding techniques that will increase resistance to diseases without compromising production efficiency and product quailty. This will require cooperation of immunogeneticists, veterinarians and animal and poultry breeders. Significant progress in the improvement of resistance to diseases may result from the application of new techniques of molecular genetics and cell manipulation.
Transmissible lymphoid tumor (TLT) was inoculated in wing webs of five-week-old chickens of 6 strains. About half of the chickens of each strain had been vaccinated with turkey herpesvirus (HVT) one week before challenge in the wing web with TLT. Tumors which developed at the site of inoculation usually reached maximum size within 2 weeks and then regressed. In some chickens, however, tumors developed in visceral organs and caused death in the 2nd through 5th weeks postinoculation. Comparisons among strains of chickens in Expt. 1 revealed no differences in mortality. Vaccination with HVT reduced mortality and also the incidence of wing-web tumors (WWT) in all strains of chickens. A lymphoid leukosis virus and a Marek's disease (MD) virus of low virulence were detected in preparations of TLT, and it is suggested that the immunity induced by vaccination may have been directed against tumor antigens associated with MD virus.
In order to gain insight into transmission and pathogenesis of infection, specimens from laying hens that had been naturally exposed to lymphoid leukosis virus (LLV) were tested for group-specific antigen (gsa) of the virus by immunofluorescence (IF), complement fixation (CF), and the enzyme-linked immunosorbant assay (ELISA). Electron microscopic examinations determined the distribution of C-type virus particles in tissues, and the phenotypic-mixing test served as a biological assay for exogenous LLV. The IF gsa was found in all organs tested, and fluorescence was usually found where virus particles were concentrated. In the oviduct and intestine, IF gsa was frequently at the border of the lumina and in the connective tissue associated with basal membranes of glands. In skin, the antigen was detected in smooth muscle, in feather pulp, and in basal epidermal cells of developing feathers. Results of various tests on Ottawa strains of chickens were usually in agreement. For example, among hens that shed gsa into egg albumen, only the viremic hens were consistently positive for IF gsa in both spleens and oviducts. Geometric mean CF titers of antigen were respectively five- and 23-fold higher in spleens and oviducts from viremic hens than in those from nonviremic hens. These findings suggest that the gsa was associated with exogenous virus infection. In Cornell S strain hens that had not been exposed to LLV, gsa was detected in splenic tissue by CF and ELISA but not by the IF test. This gsa was presumed to be of endogenous origin.
The purpose of this study was to improve in vitro procedures for detecting cellular resistance to the avian leukosis-sarcoma group of viruses. Four feather pulp organ cultures (FPOC) were prepared from each chicken by placing pulp squeezed from feathers in wells of microtitre plates that contained culture medium. Two of the four FPOC were inoculated with Rous sarcoma virus (RSV) of subgroup A and 5 to 6 days later the fluids from all four cultures were assayed for virus by inoculating chicken embryo fibroblasts (CEF) and examining for development of foci of transformed cells. Prior to the second assay of culture fluids, quail cells transformed by envelope-defective RSV [R(-)Q cells] were added to some RSV-inoculated and uninoculated FPOC. The R(-)Q cells produce infectious RSV when infected with avian leukosis virus (ALV), and hence made it possible to detect ALV in FPOC. Status of host infection was also assessed by tests for virus neutralising antibody and the enzyme-linked immunosorbent assay for group specific viral antigen. In one experiment FPOC from chickens not exposed to ALV were susceptible to RSV throughout the 140-day test period. In contrast, FPOC from ALV-inoculated chickens were usually infected with ALV and were resistant to RSV. FPOC from chickens reared in contact with the inoculated group for 121 days were free of ALV and were unexpectedly resistant to RSV. Two other experiments supported the observation that genetically susceptible chickens acquire cellular resistance to RSV as a result of persistent or transient ALV-infection. In Cornell K strain chickens there was close agreement between cellular susceptibility based on tests on FPOC prepared prior to inoculation of chickens with ALV and for antibody following inoculation with ALV. A New Hampshire strain showed a high degree of genetic cellular resistance by these test procedures.
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