Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/15/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: Breeding stocks of poultry may be susceptible or resistant to infection by a form of endogenous virus (EV) that can also be inserted into their hereditary chromosomal DNA. If experimental chickens have susceptibility to EV - and are exposed to infectious EV - then they often develop problems if grown in an environment containing a related infectious avian leukosis virus (ALV). The ALV infection of birds containing EV results in prolonged viremia affecting productivity, and may result in tumor development and death. An antiserum was developed that could be used in a simple test with blood cells to identify if chickens were susceptible to EV infection. This antiserum is valuable for defining EV susceptibility in chickens and in understanding EV infection. When this antiserum was used to identify EV susceptibility in experimental chickens exposed to ALV there was a correlation between EV susceptibility and prolonged ALV viremia and tumor development. However, this correlation was not demonstrable using commercial strain chickens that had numerous EVs. Reasons for the failure of EV susceptibility to influence economically important ALV traits in the commercial strain are discussed.
Technical Abstract: An alloantiserum, termed R2, specifically agglutinates red blood cells (RBC) from line 100B chickens that are susceptible to avian leukosis viruses (ALV) belonging to subgroups B and E, but does not agglutinate RBC from congenic inbred line 72 chickens that are resistant to ALV B and E. The R2 antigen was also detected on lymphocytes and thrombocytes. Using chickens from a special cross, it was found that R2 reactivity requires that the chickens must: 1) be susceptible to infection by ALV-E; and 2) express a viral envelope gene with subgroup E specificity. With R2 antiserum, a nearly perfect association was observed between agglutination and susceptibility to ALV-B in F2 chickens containing endogenous viral genes ev2 and/or ev3. These results support earlier evidence that ALV-B and ALV-E share receptors. Moreover, the R2 antiserum was shown to neutralize ALV-E. The R2 antigen showed Mendelian segregation in chickens of a commercial White Leghorn strain-cross containing ev3, ev6, and ev9. However, commercial chickens with or without the R2 antigen did not differ in susceptibility to lymphoid leukosis induction or immune response on infection with ALV of subgroup A for complex reasons we discuss.