HPRS‐103: A retro virus strikes back. The emergence of subgroup J avian leukosis virus

Abstract

In 1988, a new strain of avian leukosis virus (ALV) was isolated from meat-type chickens in the UK. Studies on the prototype virus strain, HPRS-103, placed it in a new envelope subgroup, designated J. The envelope gene of subgroup J ALV (ALV-J) is closely related to endogenous retroviral sequences of the EAV family present in the normal chicken genome, suggesting that ALV-J is a genetic recombinant. Sequence studies on the envelope gene of various field isolates of ALV-J indicate the occurrence of frequent mutations leading to antigenic variation. Experimentally and in the field, HPRS-103 and related viruses cause predominantly myeloid leukosis (myelocytomatosis: ML) and a variety of less common tumours, with experimentally a latent period between infection and the onset of ML mortality of 9 or more weeks and a median age at death of 20 weeks. The frequency of tumours varies considerably between lines of chickens. From some cases of ML, acutely-transforming variant viruses can be isolated which are more rapidly tumourigenic. Cell tropism studies revealed that HPRS-103 has a low tropism for bursal follicle cells, but high tropism for cultured blood monocytes. ALV-J can be detected in the field using conventional ALV isolation and characterization methods. Recently, PCR assays specific for ALV-J have been developed. Serum antibodies to ALV-J can be detected using virus neutralization techniques and ELISA tests using crude antigen from ALV-J infected fibroblasts or purified antigen produced in a baculovirus system. ALV-J spreads vertically through the embryo and horizontally by contact, producing tolerant viraemic birds and immune birds, respectively. All birds of the former class are shedders and transmitters of ALV-J to their progeny, as are a few birds in the immune class. Meat-type birds infected soon after hatching are particularly prone to becoming tolerant also. Shedder hens can be identified by testing vaginal swabs and egg albumen for ALV group-specific antigen by an ELISA, allowing ALV-J eradication protocols to be designed. Commercial application of such an eradication programme over several years has resulted in a marked reduction in the prevalence of virus in infected breeding flocks.

Subgroup J avian leukosis virus infection in turkeys: Induction of rapid onset tumours by acutely transforming virus strain 966

“…These birds were nonviraemic and non-shedders (V-A+S-), similar to the layer-type chickens infected after hatching with ALV-J. However, one bird each infected with HPRS-103 and 966 virus, respectively, remained as a tolerantly viraemic shedder (V+A-S+), an infection status seen commonly in meat-type chickens infected with ALV-J (Payne, 1998). It has been proposed that embryonic expression of EAV-HP env-like sequences might contribute to the development of tolerance against ALV-J in meat-type chicken .…”

“…ALV-J infection is recognized currently as a major disease problem affecting the broiler breeder chicken industry worldwide (Payne, 1998). Although layer-type chickens are experimentally susceptible to infection with these viruses, so far ALV-J-associated tumour mortality has been restricted largely to the meat-type chickens.…”

“…HPRS-103 is a replication competent virus that induces tumours by mechanisms such as promoter insertion near oncogenic sequences (Payne, 1998). Induction of tumours by this mechanism is a slow process and it was not very surprising that the infected birds did not develop tumours during the 10-week experimental period.…”

The oncologist's debt to the chicken

“…Once again, Jim Payne's ALV research happens to provide useful information on this potential problem. The HPRS-103 leukosis virus has an env gene derived from EAV (Payne, 1998). While EAV particles themselves have not been shown to be infectious, the host range of HPRS-103 can be tested.…”

Histopathological and ultrastructural characteristics of myeloid leukosis in broiler chicken

“…Some authors state that in myeloid leukosis the neoplastic cells are originated from the myelomonocytic lineage at the final stage of differentiation, myelocytes or monocytes (Payne, 1998), while others postulate that the origin may be in the myeloblasts (Jordan and Pattison, 1996). An experimental inoculation of the virus in a bone marrow cell culture showed that the transformed cells had morphologic features suggestive of macrophage precursor cells (Payne et al, 1993).…”