Progress towards eradication of lymphoid leukosis viruses ‐ A review

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.

Section: Eradication Of Alv-j In the Fieldmentioning

confidence: 99%

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

Payne

1998

“…Traditional virus isolation procedures and IFA identi® cation are generally not used to identify ALV infections in commercial poultry¯ocks because these assays require about 2 weeks to determine viral infection. Currently, the poultry industry uses an ELISA assay to screen for ALV GSA in infected chickens (Spencer, 1984(Spencer, , 1987. Since both exogenous and endogenous ALV exhibit common GSA, ELISA assays cannot be used reliably to discriminate between GSA of exogenous and endogenous origin.…”

Section: Introductionmentioning

confidence: 99%

Detection of exogenous and endogenous avian leukosis virus in commercial chicken eggs using reverse transcription and polymerase chain reaction assay

Pham¹,

Spencer²,

Traina‐Dorge³

et al. 1999

Avian leukosis retroviruses (ALV) cause lymphomas and other cancers in chickens.Previous studies have used enzyme-linked immunosorbent assays (ELISA) and indirect immuno¯uorescence assays (IFA) to detect ALV p27 group-speci® c antigens (GSA) in commercial chicken eggs. In the poultry industry eradication programme against exogenous ALV, ELISA assays are used to identify chickens infected with the virus. The inability of ELISA and IFA assays to discriminate between ALV GSA of endogenous or exogenous origin, and actual virus, have limited rigorous assessments of viral transmission dynamics. Here, we report the use of a newly developed reverse transcriptase-polymerase chain reaction (RT-PCR) assay, with direct sequencing of the RT-PCR product, to show endogenous and exogenous ALV in albumen from unfertilized chicken eggs. We found that 95% of 20 eggs from ALV-exposed commercial chickens and 14.2% of 240 egg samples from 20 randomly chosen New Orleans retail stores were ALV-positive by RT-PCR. In comparison, only 2.5% of the same egg samples from the retail stores were positive by ELISA. Corresponding direct sequencing of randomly chosen RT-PCR products showed that four of six egg samples contained endogenous ALV, while two of the six samples were positive for exogenous subgroup A ALV. The ® nding of endogenous subgroup E ALV in unfertilized chicken eggs emphasizes that the transmission of endogenous ALV is common and should be considered in the implementation of ALV eradication programmes by the poultry industry.

“…Eliminating such hens as breeders has been effective in reducing the incidence of infection in subsequent generations (Spencer, 1984;deBoer, 1986). While endogenous viral genes are common in White Leghorns, there is usually limited replication of complete virus.…”

Section: Introductionmentioning

confidence: 99%

Endogenous leukosis viral antigen in eggs from meat‐type chickens on an avian leukosis virus eradication programme

Spencer¹,

Chambers

1992

SUMMARYIn an effort to eliminate exogenous avian leukosis virus (ALV) from a susceptible population, albumen of one egg per hen from each of four generations was tested by ELISA for groupspecific antigen (gsa) of leukosis/sarcoma viruses. From 1510 to 2099 hens were tested in each generation. Hens were not used as breeders if optical density readings for gsa were 0.4 or greater. Despite this procedure, there was no appeciable change in the occurrence of gsa in eggs from one generation to the next and in the sire population the percentage of hens with levels of 0.4 or greater was 7.1 and 8.7 in the first and fourth generations tested, respectively. There were no consistent differences in antigen levels in any of the eight strains that comprised the two populations.For the most part, antigen detected in eggs resulted from expression of endogenous viral genes since there was a low incidence of exogenous infection. Six of 234 hens of the second generation tested from the sire population were positive for ALV in serum and three of 161 were positive for antibody to subgroup A virus; no antibody to subgroup B was detected. Five of the six hens that tested positive for ALV were from the same strain and had been reared together. With one exception these hens would have been eliminated as breeders based on tests for antigen in eggs. In the fourth generation tested, no virus or subgroup A antibody was found in serum from approximately 250 hens from the two populations.