Amyloid A amyloidosis in non-infected and avian leukosis virus-C persistently infected inbred ducks

Abstract

The breeding history of the first inbred strain of Khaki Campbell ducks is presented. The genetic homogeneity of this strain was tested on the basis of serum amyloid A (SAA) polymorphism and it was established that it harbours only the SAA allele A, which is expressed in liver, lung and bursa of Fabricius tissues. Pathogenic changes in control and avian leukosis virus-C (ALV-C) persistently infected ducks were evaluated during the period spanning 1 to 10 months after hatching. In both groups, AA amyloidosis was revealed and characterized. In spite of the inbred nature of animals, the incidence of amyloid A deposition varied among experiments, suggesting that additional non-genetic factors are involved. Similar variation was found in ALV-C persistently infected ducks, where only in one out of three experiments was the incidence of AA amyloidosis significantly higher than in controls.

Identification of two novel multiple recombinant avian leukosis viruses in two different lines of layer chicken

“…ALV-C has cytopathogenicity in cultured DF-1 cells (Himly et al, 1998). In recent years, ALV-C has often been used as a comparative system for establishing pathways leading to immunodeficiency syndrome in both homologous and heterologous hosts (Stepanets et al, 2001(Stepanets et al, , 2003.…”

Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J

“…North American and Asian duck populations share wintering grounds, and at least two reports indicate the presence of ALV-J in ducks and partridges (17,18). Avian leukosis viruses of other subgroups can infect ducks and establish persistent infections in these heterologous hosts (38,39). On the other hand, we reported that NHE1 receptors of duck species are restrictive, and in vitro infection of duck embryo fibroblasts with ALV-J was inefficient (21).…”

Differences in pathogenicity among strains of the same or different avian leukosis virus subgroups

“…(For virus strains, see Table 2.) Viruses were grown on the chicken embryo fibroblast cell line DF-1 (Himly et al, 1998) except for subgroup C viruses, which were propagated on duck embryo fibroblasts (isolated from inbred Khaki Campbell ducks of the D/ABDE phenotype from the breeding colony of the Institute of Molecular Genetics; Stepanets et al, 2001). As measured by the 16Q test (see below), standard production of 10 6 to 10 7 infectious units (IU)/ml was obtained with all virus strains.…”

“…Determination of body and organ mass and immunohistochemistry of lymphoid tissues 2 weeks after hatching Table 4 11 Proliferative response to conA stimulation of splenocytes isolated from 2-week-old chickens inoculated in mid embryogenesis with RAV-1 or td daPR-C Table 6 12 Humoral immune response to B. abortus antigen of chickens inoculated in mid embryogenesis with RAV-1 or td daPR-C and repeatedly immunized in the period 2 to 8 weeks after hatching Table 7 Determination of the replicating virus in plasma. The presence of infectious virus in chicken plasma was determined by the complementation test with 16Q cells (quail cells harbouring the provirus of high-titre Bryan strain Rous sarcoma virus lacking the env gene) (Murphy, 1977), essentially as described previously (Stepanets et al, 2001). Briefly, chicken embryo fibroblasts were incubated with 100 ml chicken plasma, subcultured twice and co-cultivated with 16Q cells for 1 week.…”