Differential mortality and lesion responses to reticuloendotheliosis virus infection in Marek's disease-resistant and susceptible chicken lines

Abstract

The major histocompatibility complex of the chicken (Pazderka et al. 1975) resembles the mouse H-2 region in controlling many phenomena related to adaptive immune responsiveness. Immune response (Ir) loci within the B complex control cell-mediated and humoral immune responses to defined antigens (G/inther et al. 1974, Benedict et al. 1975, 1977). Lymphocyte response in the graft-versus-host and mixed lymphocyte reactions is also controlled by the B locus (Longenecker et al. 1972, Miggiano et al. 1974). Strain differences in host response to infection by Marek's disease virus (MDV) or avian leukosis virus (ALV) are well documented. Chickens heterozygous or homozygous for the B 21 allele show resistance to T-cell lymphomagenesis by MDV (Longenecker et al. 1976, Briles et al. 1977). Differences between chicken lines in regression of tumors induced by Rous sarcoma virus (Schierman et al. 1977, Collins et al. 1977), and susceptibility to induction of lymphoid leukosis (LL), a B-cell lymphoma, after ALV infection have also been described (Purchase and Gilmour, 1975, Crittenden et al. 1972). Reticuloendotheliosis virus (REV), the prototype of a newly described group of avian C-type retroviruses (Purchase et al. 1973), induces tumors composed of undefined hematopoietic cells in the spleen and liver in experimentally infected chickens (Purchase and Witter 1975). REV differs markedly from other avian tumor viruses in its virulence. The induction period may be as short as 5 days, and mortality may approach 100% (Purchase and Witter, 1975). REV induces the only 'short-incubation' lymphoreticular tumor caused by an avian C-type retrovirus, and therefore offers an attractive avian model system for studies of genetic control of tumorigenesis. The present report describes differences in mortality patterns and visceral lesion development in line N and line P chickens (B-locus genotype B21/B 21 and B19/B 19, respectively). These lines were developed by Cole (1972) on the basis of resistance and susceptibility to Marek's disease (MD). Differences between line N and P chickens in response to MDV infection may reflect genetically determined differences in the immune responses to virus infection and tumorigenesis (Briles et al. 1977). To investigate the possibility of genetic control of tumorigenesis in the REV system, we compared the mortality patterns and lesion responses of these two lines to REV infection. Chickens of line N (BZI/BEI) and line P (B19/B 19) were hatched on the same day and were inoculated intraperitoneally with REV (0.1 ml containing 5 • 103 plaque-