Resistance of line 6₃ chickens to reticuloendotheliosis‐virus‐induced bursa‐associated lymphomas

Abstract

Chickens of lines 6(3) and 151(5) X 7(1) were inoculated with the chick syncytial strain of reticuloendotheliosis virus (REV) or with the Rous-associated virus-I of avian leukosis virus (ALV) at hatching. At 4, 10, 16, and 36 weeks post inoculation (PI), chickens were tested for REV- and ALV-induced viremia and antibody. The incidence of REV- or ALV-induced bursa-associated lymphomas in line 6(3) chickens was compared with that in line 151(5) X 7(1) chickens. Inoculation of REV at hatching resulted in immunological tolerance to the virus in line 6(3) but not in line 151(5) X 7(1) chickens. Between 70% and 100% of line 6(3) chickens remained viremic and lacked REV antibody throughout the experimental period of 36 weeks. In contrast, ALV-inoculated chickens of both lines had antibody by 16 weeks PI. The frequencies of REV- and ALV-induced bursa-associated lymphomas in line 6(3) chickens were significantly lower than in line 151(5) X 7(1) chickens. Further, the incidence of bursa-associated lymphomas induced by REV in line 151(5) X 7(1) chickens was significantly lower than that induced by ALV. These results suggest that: (1) the genetic constitution of the host may influence the immunological response to REV infection; (2) chickens resistant to ALV-induced bursa-associated lymphomas are equally resistant to such lymphomas induced by another unrelated avian retrovirus, REV; and (3) ALV is a more potent inducer of bursa-associated lymphomas than REV.

In vitro rapid clearance of infectious bursal disease virus in peripheral blood mononuclear cells of chicken lines divergent for antibody response might be related to the enhanced expression of proinflammatory cytokines

“…Exploitation of available chicken genetic resistance to pathogens has been adjudged as best strategy for the control and prevention of disease. Many studies on infectious diseases in birds provided evidence for genetic differences in susceptibility (Fadly and Witter, 1986;Girard-Santosuosso et al, 1998;Ignjatovic et al, 2003). Comparisons between inbred lines of chickens show large differences in susceptibility of different genotypes to IBD.…”

Transcriptional Profiling Reveals a Possible Role for the Timing of the Inflammatory Response in Determining Susceptibility to a Viral Infection

“…While the poultry industry is now the most important source of animal proteins for the human diet, it is facing increasing problems from progressively more virulent forms of pathogenic viruses. Many studies have documented the existence of genetically determined differences in resistance to infectious disease in chickens (16,19,25,35), but there is little knowledge of the mechanisms responsible. Recent outbreaks of avian influenza and severe acute respiratory syndrome emphasize the threat from emerging disease carried by domestic animals.…”

“…Live IBDV vaccines can control infection but are imperfect, and this control is threatened by the emergence of increasingly virulent IBDV strains (9,15,36). A study of IBDV infection in older birds provided evidence for genetic differences in susceptibility (16). The line BrL was highly susceptible to IBDV infection, with a mortality rate of 80% 8 days after infection, despite being one of the most robust lines when facing many other diseases (5,6).…”

Reduced Myc overexpression and normal B-cell differentiation mediate resistance to avian leukosis virus lymphomagenesis

“…The overall levels of virus infection are similar in REV-infected susceptible and resistant birds (Fadly and Witter, 1986), while Marek's virus infection is reduced in resistant Line 6 3 birds (Lee et al, 1981). A viral transcription defect could potentially also be involved in resistance to tumor induction by these viruses.…”