Leukosis Virus Infection Research Articles

Detection and Characterization of Avian Leukosis Virus in Marek's Disease Vaccines

Avian leukosis virus (ALV) infection in chickens is known to induce increased mortality, tumors, delayed growth, and suboptimal egg production. Countries importing specified pathogen-free eggs, vaccines, and poultry breeding stock require freedom of infection or contamination with ALV in such products among other avian pathogens. Recently, ALV was found as a contaminant in a limited number of commercial poultry vaccines, even after routine quality assurance procedures cleared the vaccines for commercialization. The contaminated vaccines were promptly withdrawn from the market, and no direct detrimental effects were reported in poultry vaccinated with such vaccines. We describe herein the characterization in vitro of the contaminant viruses. All exogenous viruses detected in four vaccine lots belong to subgroup A of ALV based on cell receptor interaction, subgroup-specific polymerase chain reaction (PCR), envelope gene sequencing, and virus neutralization. A combination of thermal treatment and serial dilutions of the contaminated vaccines facilitated detection of contaminating ALVs in cell culture coupled with antigen-capture enzyme-linked immunosorbent assay. Subgroup-specific PCR readily detected ALV-A directly in the contaminated vaccines but not in naive vaccines or cell controls. Our methods are proposed as complementary procedures to the currently required complement fixation for avian leukosis test for detection of ALV in commercial poultry vaccines.

Single and concurrent avian leukosis virus infections with avian leukosis virus-J and avian leukosis virus-A in Australian meat-type chickens

Australian broiler breeders were screened for avian leukosis viruses (ALVs) (May 2001 to December 2003) as surveillance of measures to reduce the prevalence of ALV-J. Samples of blood (4233), albumen (1122), meconium (99) and tumours (16) were obtained from 93 flocks in six Australian states. Virus isolation was performed in C/O chick embryo fibroblast cultures, which were initially screened by group-specific antigen enzyme-linked immunosorbent assay, with follow-up confirmation using polymerase chain reaction. The chronology of isolations reveals the circulation of both ALV-J and ALV-A during this period. On 16 occasions single isolations were found to contain both ALV-A and ALV-J. This is the first report of dual infections with two subgroups of ALV occurring in the same chicken. The effectiveness of ALV-J eradication measures is indicated by the absence of any ALV-J isolations in late 2003. ALV-A however, continued to be isolated from the broiler population. The detection of dual infections, as well as the ongoing occurrence of ALV-A in meat-type birds, is discussed in the context of ongoing potential for recombinations and the associated threat for the emergence of avian leukosis virus with changes in host range and pathogenicity.

Detection of subgroup J avian leukosis virus infection in Australian meat‐type chickens

To determine the extent of avian leukosis virus subgroup J (ALV-J) infection in Australian broiler breeder flocks, using virus isolation and molecular biological detection. Any resultant ALV-J viral isolates to be characterised by neutralisation cross testing in order to determine antigenic relationships to overseas isolates of ALV-J. Samples of blood, feather pulp, albumen and tumours were obtained from broiler breeder flocks which represented four genetic strains of meat chickens being grown in Victoria, South Australia, NSW and Queensland. Dead and ailing birds were necropsied on farm and samples were collected for microscopic and virological examinations. Virus isolation was carried out in C/O and DF-1 CEF cultures and ALV group specific antigen was detected in culture lysates using AC-ELISA. Micro-neutralisation assay was used for antigenic characterisation of selected isolates. Genomic DNA was isolated from cultured cells, tumours and feather pulp. ALV-J envelope sequences were amplified by PCR using specific ALV-J primers while antibodies against ALV-J were detected by ELISA. A total of 62 ALV-J isolates were recovered and confirmed by PCR from 15 (31.3%) of 48 breeder flocks tested. Antibody to ALV-J was detected in 20 (47.6%) of the 42 flocks tested. Characteristic lesions of myeloid leukosis caused by ALV-J were found in affected flocks. The gross pathological lesions were characterised by skeletal myelocytomas located on the inner sternum and ribs, neoplastic enlargement of the liver, and in some cases gross tumour involvement of the spleen, kidney, trachea, skeletal muscles, bone marrow, skin and gonads. Microscopically, the tumours consisted of immature granulated myelocytes, and were present as focal or diffuse infiltrations in the affected organs. Virus micro-neutralisation assays demonstrated antigenic variation among Australian isolates and to overseas strains of ALV-J. ALV-J infection was prevalent in Australian broiler breeder flocks during 2001 to 2003. Australian isolates of ALV-J show a degree of antigenic variation when compared to overseas isolates.

P‐82 Mycosis fungoides in a cow with bovine leukosis virus

Mycosis fungoides (MF) is a cutaneous manifestation of a T‐cell lymphoma, which has been diagnosed in various species including one case in a 10‐month‐old calf. However, we are not aware of a case report of MF in an adult bovine or of this disease being associated with bovine leukosis virus infection. We report a case of a cow diagnosed with MF‐like disease and bovine leukosis virus. A 6‐year‐old Holstein cow was presented with a history of cutaneous masses, anorexia, weight loss and reduced milk production. This cow had delivered a healthy calf 49 days before admission. Two days before parturition, the owner had observed the first skin nodules, which had progressively enlarged. Physical examination revealed multiple alopecic hyperpigmented tumors, ranging from 2 to 7 cm in diameter, which were painful on palpation. Some of the lesions were ulcerated, although most were covered by dry and rough epidermis. No abnormality other than the skin lesions and emaciation was detected on clinical examination. Complete blood count revealed leukocytosis (23,450/μL), lymphocytosis (17,588/μL) and atypical lymphocytes. Plasma protein concentration was 6.8 g/dL. Agar gel immunodiffusion test for bovine leukosis virus was positive. Histopathological findings included a diffuse dermal lymphocytic infiltration and epitheliotropism. Immunohistochemistry revealed that neoplastic lymphocytes were CD3+ and CD79a– cells. Due to the poor prognosis, the cow was euthanized. This report describes a rare MF d’emblée‐like condition in a cow with bovine leukosis virus. Funding: Self‐funded.

The effects of cyclophosphamide treatment on the pathogenesis of subgroup J avian leukosis virus (ALV-J) infection in broiler chickens with Marek's disease virus exposure

Studies were performed to determine the effects of Bcell suppression on the pathogenesis of Subgroup J avian leukosis virus (ALV-J) in broiler chickens. Neonatal chickens were treated with cyclophosphamide (CY) or PBS, and then infected with ALV-J (ADOL-7501) at 2 weeks of age. CY treatment induced B cell specific immunosuppression throughout the experiment confirmed by decreased bursal weight, intact lymphocyte mitogenetic activity stimulated by Con A and increased relative subpopulation of CD3-positive cells as measured by flow cytometry. Chickens in this experiment had Mareks disease virus exposure prior to three weeks of age as determined by the presence of lymphocytic infiltration and antibody. Virus neutralizing antibody against ALV-J was first observed at 6 weeks post-infection in some of the infected chickens in the PBS group. As expected, none of the chickens from the CY group and uninfected chickens developed virus-neutralizing antibody. The viremic status was measured by real time RT-PCR using SYBR green I dye. The percentage of viremic chickens was significantly higher, and more chickens had high titered viremia, in the CY treated group. No neoplastic foci consistent with ALVJ infection were observed in any of the experimental chickens. The frequency and intensity of viral antigen expression determined by immunohistochemistry was significantly higher in tissues from CY treated birds than those of PBS treated chickens at 3 weeks post-infection. This study showed that B cell specific immunosuppression with CY treatment in chickens resulted in increase in viremia and viral antigen load in tissues.

Eradication of enzootic bovine leukosis from Finland

Enzootic bovine leukosis (EBL) was recognized among Finnish cattle in 1966. Administrative decisions specifying and refining official control measures were given in 1966, 1976, 1980, and 1993. The measures' key principle always has been 'test and slaughter'. The EBL/bovine leukosis virus (BLV) infection situation was monitored at meat inspection, and hematologically between 1970 and 1977 and serologically between 1978 and 1989. Annual surveys including all dairy herds and samples from beef animals were conducted in 1990-2001. Bulk-tank milk samples represented the dairy herds in the surveys; the beef animals were sampled individually at slaughter. The maximum positive herd-level percentage in the surveys was 0.03%. EBL/BLV infection was evenly dispersed in the southern part of the country and nonexistent in the northern part. We conclude that herd-level prevalence of EBL/BLV infection never exceeded 5%. It nevertheless took 30 years to eradicate the disease and the infection. EBL was eradicated from mainland Finland in 1996 and from the island district of Ahvenanmaa in 1999. Annual monitoring of the EBL situation continues.

Occurrence of subgroup J avian leukosis virus in Taiwan

There are three grandparent farms for three different chicken breeds in Taiwan. One of these farms, populated by breast meat yield chickens (yield type), suffered from a severe subgroup J avian leukosis virus (ALV-J) infection in mid-1997. The affected flocks at that farm had a weekly mortality of more than 1% and a 15% drop in egg production. The broilers from that breed had a 10% condemnation rate during the first week of age, and 5% of the remaining broilers were stunted afterwards. Some chickens had myeloid leukosis lesions at 6 weeks old. Their survivability was about 85%. However, chickens at the other two grandparent farms, populated with non-yield chickens (regular type), were also infected by ALV-J and showed myeloid leukosis. However, chickens at these farms produced progeny whose survivability reached more than 95%. ALV-J caused greater economic loss in yield type chickens than in regular type chickens in Taiwan.

Cardiomyopathy in broiler chickens congenitally infected with avian leukosis virus subgroup J.

Dilated cardiomyopathy and ascites in broiler chickens are frequently associated with rapid growth and pulmonary hypertension, but can be associated with some avian leukosis virus (ALV) infections. The novel subgroup J of ALV has a high cardiac tropism, but dilated cardiomyopathy has not been reported previously. We report a dilated cardiomyopathy incidence of 11.1% in broiler chickens congenitally infected with ALV subgroup J (ALV-J). Gross lesions included severe body weight suppression, cardiomegaly with biventricular dilation, right ventricular hypertrophy, visceral congestion, and ascites. Cardiac myocytes and Purkinje fibers contained 2- to 10-microm intracytoplasmic magenta inclusions that contained ALV-J-specific nucleic acid. Ultrastructurally, inclusions contained ribosomes and immature virions and were associated with myofibril disruption and disarray. Peracute centrilobular hepatic necrosis was present in most cases. ALV-J-associated cardiomyopathy may involve a direct viral effect on cardiac myocytes and Purkinje fibers.

Resistance to Marek's Disease Virus in White Leghorn Chickens: Effects of Avian Leukosis Virus Infection Genotype, Reciprocal Mating, and Major Histocompatibility Complex

Genetic improvement for resistance to Marek's Disease (MD) in chickens continues to be of interest to the poultry industry. The aims of this study were to identify effects of the MHC on the molecular level and of avian leukosis virus (ALV) resistance status on MD mortality in two noninbred White Leghorn chicken lines that differ in B blood group type. Previously, within each of the chicken lines, sublines had been selected for resistance or susceptibility to ALV infection with Subgroups A and B. In this study, F2 offspring, obtained by crossing the two ALV-resistant or the two ALV-susceptible sublines, were tested for MD mortality after contact exposure at 1 d of age. Reciprocal matings were made in the grandparental generation. The MD mortality percentages, in an observation period of 17 wk, of F2 offspring from two hatches were 82.63 and 92.35%, respectively. Survival analysis (Cox model) was applied to assess the risk of dying from MD. No differences in MD mortality risk profiles were found between ALV-resistant and ALV-susceptible F2 offspring. Within ALV-susceptible F2 offspring, however, a reciprocal mating effect was observed in both hatches. The MHC Class I, II, and IV restriction fragment length polymorphism (RFLP) analyses were carried out on birds of the first hatch. Although two of 11 MHC class IV RFLP bands displayed a significant effect, in general, a strong association of MHC and MD mortality was not detectable.

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

Avian leukosis virus subgroup J (ALV-J), isolated in the late 1980s, predominantly causes myelocytic myeloid leukosis in meat-type chickens. In the past 10 years, ALV-J infection has become very widespread, causing serious problems to the chicken meat industry. Previously, we have shown that turkey cells can be infected in vitro with Rous sarcoma virus pseudotypes of ALV-J. In this paper, we extend those observations to show that turkey monocyte cultures can be transformed in vitro with acutely transforming ALV-J strain 966. We also show that turkeys are experimentally susceptible to infection with ALV-J prototype strain HPRS—103. However, neoplastic lesions were not observed in these birds, probably due to the short experimental period of 10 weeks. When inoculated into 1-day-old turkey poults, acutely transforming ALV-J strain 966 induced tumours between 3 and 4 weeks after infection. Most of the birds showed tumours involving the liver, with histopathological lesions of myelocytomatosis. The demonstration of the spread of HPRS—103 by contact among turkeys, although observed only at low levels in the present study, stresses the importance of segregation of turkey and chicken breeding operations to avoid the spread of ALV-J infection.

A Genetically Engineered Cell Line Resistant to Subgroup J Avian Leukosis Virus Infection (C/J)

A cell line (DF-1¿J) expressing the envelope protein isolated from the ADOL-Hc1 strain of the avian leukosis virus subgroup J (ALV-J) was used to analyze receptor interference to six different isolates of ALV-J as well as ALV subgroups A-D. The traditional gag-specific enzyme-linked immunosorbent assay (ELISA) as well as flow cytometry was used to evaluate viral infection. The parental cell line (DF-1) was susceptible to all ALV subgroups tested while the DF-1¿J cell line was selectively resistant to the subgroup J isolates. The DF-1¿J cell line was resistant to infection by all six ALV-J isolates as determined using the gag-specific ELISA. There was no interference with the other ALV subgroups (A-D) induced by the expression of the ADOL-Hcl envelope. The ALV-J isolates used in this analysis are serologically distinct when analyzed by flow cytometry. Convalescent sera to ADOL-Hcl cross-reacts with all of the ALV-J isolates tested; however, sera to HPRS-103 did not bind to four of the six isolates. Based on the intensity and differential binding of these antisera using flow cytometry, the six ALV-J isolates used can be grouped into four categories. Thus the DF-1¿J cell line is resistant to infection by a serologically and genetically diverse group of ALV-J isolates and should be useful as a diagnostic tool.

Genetic analysis of Rous sarcoma virus (subgroup A) induced tumourigenesis and performance of synthetic broiler stocks in relation to group-specific antigen shedding

An investigation was made using two high-performance meat lines, synthetic male line (SML) and synthetic dam line (SDL), to assess the susceptibility pattern in response to subgroup A Rous sarcoma virus (RSV) and the effect of group-specific (gs) antigen shedding in eggs, as evidence of avian leukosis virus infection effects on production and fitness traits. The ar gene frequency was observed to be at 0.68 +/- 0.04 and 0.66 +/- 0.06 for SDL and SML lines, respectively. Synthetic broiler lines were fivefold less sensitive to pock expression in chorioallantoic membranes (CAMs) as compared with a White Leghorn (WL-2A) reference line, in response to Bryan standard RSV (subgroup A). It was also observed that gs antigen shedding had neither influence on pock response in CAMs nor on induced liver tumour death. The prevalence of gs antigen shedding, however, fluctuated from generation to generation, ranging from 16.66 to 69.23% in SDL and 20.68 to 51.85% in SML, indicating an exogenous infection. Analysis of the relationship of gs antigen shedding in eggs with some fitness traits and overall flock production traits provided strong evidence that fitness traits such as fertility, hatchability, and production traits, such as 6-week body weight and egg weight, were significantly influenced by gs shedding.

Differential selection of cells with proviral c-myc and c-erbB integrations after avian leukosis virus infection.

Avian leukosis virus (ALV) infection induces bursal lymphomas in chickens after proviral integration within the c-myc proto-oncogene and induces erythroblastosis after integration within the c-erbB proto-oncogene. A nested PCR assay was used to analyze the appearance of these integrations at an early stage of tumor induction after infection of embryos. Five to eight distinct proviral c-myc integration events were amplified from bursas of infected 35-day-old birds, in good agreement with the number of transformed bursal follicles arising with these integrations. Cells containing these integrations are remarkably common, with an estimated 1 in 350 bursal cells having proviral c-myc integrations. These integrations were clustered within the 3' half of c-myc intron 1, in a pattern similar to that observed in bursal lymphomas. Bone marrow and spleen showed a similar number and pattern of integrations clustered within 3' c-myc intron 1, indicating that this region is a common integration target whether or not that tissue undergoes tumor induction. While all tissues showed equivalent levels of viral infection, cells with c-myc integrations were much more abundant in the bursa than in other tissues, indicating that cells with proviral c-myc integrations are preferentially expanded within the bursal environment. Proviral integration within the c-erbB gene was also analyzed, to detect clustered c-erbB intron 14 integrations associated with erythroblastosis. Proviral c-erbB integrations were equally abundant in the bone marrow, spleen, and bursa. These integrations were randomly situated upstream of c-erbB exon 15, indicating that cells carrying 3' intron 14 integrations must be selected during induction of erythroblastosis.

Role of contact and genetic transmission of endogenous virus-21 in the susceptibility of chickens to avian leukosis virus infection and tumors

The role of contact and genetic transmission of endogenous virus-21 (EV21) on response of chickens to avian leukosis virus (ALV) infection and tumors was studied. F1 progeny of a cross between RPRL late-feathering (LF) line EV21+ males and RPRL early feathering (EF) line 15B1 females harboring or lacking EV21 were used. The EF chicks lacking EV21 were inoculated with a field strain of subgroup A ALV at hatch and contact exposed to LF, EV21+ hatchmates for various time intervals. In a second experiment, EV21 contact-exposed and unexposed EF chicks as well as LF, EV21+ hatchmates were inoculated with ALV at various ages. Chickens were tested for ALV-induced viremia and antibody and were observed for tumors until 24 wk of age. Antibody to EV21 in EF chickens contact-exposed to LF, EV21+ hatchmates varied from 10 to 65%, and was detected by 10 wk of age. By 24 wk of age, ALV-induced viremia and tumors in EF chickens varied from 5 to 30%, and from 15 to 32%, respectively, regardless of exposure to EV21. The incidence of ALV-induced tumors was significantly higher in LF chickens genetically infected with EV21 than in EV21 contact-exposed or unexposed EF chickens, but only in chickens inoculated with ALV at hatch. The data suggest that contact infection with EV21 has no influence on ALV infection and tumors. The data also suggest that genetic transmission of EV21 may increase susceptibility of chickens to ALV infection and tumors following infection with ALV at hatch, but not at 4 wk of age or older.

Serological evidence of the occurrence of enzootic bovine leukosis (EBL) virus infection in cattle in Tanzania.

Antibodies specific to bovine leukosis (leukemia) virus (BLV) were examined by enzyme-linked immunosorbent, assay (ELISA) in 2,849 serum sample from exotic/improved and indigenous cattle originating from 6 regions of Tanzania, 2,047 from dairy cattle and 802 from beef cattle. An overall infection rate (prevalence) of approximately 36% was detected. The infection rates were 41% and 21.4% in dairy and beef herds respectively. In the dairy herds the infection rate varied from herd to herd. The possible sources of infection and methods of spread within Tanzania are discussed.

Endogenous viral genes influence infection with avian leukosis virus

The influence of endogenous viral (ev) genes on avian leukosis virus (ALV) infection was studied in ALV-free white leghorn chickens exposed to chicks from ALV shedding dams. The study included four lines, each segregating for one ev gene, one line free of ev genes, and four commercial stocks segregating for a number of ev genes. Genes ev12 and ev21 that produce the complete endogenous virus were associated with significant reductions in antibody response to ALV. In commercial stocks with ev21 in all birds, both antibody response and ALV in oviducts were significantly influenced by the genomic background (stock). In one commercial stock, 37.6% of 133 birds with ev21 and only 5.8% of 120 birds without the gene were test-positive for virus in their oviducts at 180 days of age. No such differences were associated with ev1, ev3 or ev6 that do not produce complete endogenous virus. Thus, virus-producing ev genes were a predisposing factor for shedding ALV.

Incidence of endogenous viral genes in Leghorn strains of different origin, each with sublines of a different genotype for resistance to avian leukosis virus infection

SummaryThe identification of genes affecting disease resistance in domestic fowl has challenged research workers in various countries, in the study of their effects and in the evaluation of their potential for commercial poultry breeding. This study concerns endogenous viral genes (ev genes), which can play an important role in the response to avian leukosis virus infection.The incidence of ev genes was determined in three experimental White Leghorn strains of different origin, each consisting of two sublines genotypically either susceptible or resistant to infection from avian leukosis virus (ALV) of the subgroups A and B. The three pairs of sublines had been used extensively for investigations of the effects of leukosis infections in laying hens. Among the 11 ev genes found, only three were present in all three strains – ev1 and ev3, which appear to be very common in White Leghorn, and ev6, which has been associated with reduced immune response to ALV infection. Five of the 11 ev genes found occurred only in one of the three strains, while the number of different ev genes in each of the strains amounted to either six or seven.The frequency of each ev gene present in a strain was surprisingly similar in the genotypically resistant and susceptible subline. With the exception of ev1 and ev3, which were present in all three strains at a relatively high frequency, there were striking differences between the strains in the level of frequencies of the additional ev genes. In one of the strains, which originated from a commercial hybrid, this level was exceptionally low, while the additional ev genes had much higher frequencies in the other two strains. The information about the incidence of ev genes, and specifically that about ev6, suggested a plausible explanation for the striking difference observed between the three Leghorn strains in their respect to ALV infection and, in particular, the rate of congenital ALV infection.ZusammenfassungVorkommen von endogenen Virus‐Genen in Leghorn‐Linien verschiedenen Ursprungs, jeweils mit Sublinien interschiedlichen Genotyps für Infektionsresistenz gegen GeflügelleukoseDie Identifizierung von Einzelgenen, von denen Einflüsse auf die Widerstandsfähigkeit gegen Krankheiten beim Hausgeflügel ausgehen, haben in mehreren Ländern intensive Forschungsaktivitäten zur Untersuchung der von ihnen ausgehenden Wirkungen ausgelöst, um ihrem möglichen Nutzen für die kommerzielle Geflügelzüchtung besser bewerten zu können. Dieser Beitrag betrifft endogene Virusgene (ev Gene), die einen wesentlichen Einfluß auf die Auswirkung einer Infektion durch Geflügelleukoseviren ausüben können.Das Vorkommen endogener Virusgene wurde in drei experimentellen Linien von weißen Leghorn unterschiedlichen Ursprungs untersucht, von denen jede aus zwei Sublinien bestand, die genotypisch entweder empfänglich oder resistant gegen Infektion durch Geflügelleukoseviren (ALV) der Untergruppen A und B waren. Mit diesen drei Paaren von Sublinien waren bereits umfangreiche Untersuchungen über die Auswirkung von Leukoseinfektionen bei Legehennen durchgeführt worden. Von den insgesamt 11 identifizierten ev‐Genen kamen nur drei in alien Linien gleichzeitig vor. Dabei handelte es sich um ev 1 und ev 3, die bei weißen Leghorn häufig auftreten und ev 6, das sich negativ auf die Immunreaktion nach Infektion durch ALV auswirken kann. Von den vorhandenen ev‐Genen kamen fünf jeweils nur in einer der drei Linien vor, während sich die Anzahl verschiedener ev‐Gene pro Linie auf sechs oder sieben belief.Für jedes der in einer Linie vorkommenden ev‐Gene war deren relative Häufigkeit in der genotypisch resistenten und empfänglichen Sublinie überraschend ähnlich. Mit Ausnahme von ev 1 und ev 3, deren relative Häufigkeit in alien drei Linien besonders hoch lag, traten zwischen den Linien bei den übrigen ev‐Gene in dieser Hinsicht deutlichere Unterschiede in Erscheinung. In der Ausgangslinie, die auf eine kommerzielle Hybridherkunft zurückgeht, waren die Frequenzen ungewöhnlich niedrig, während sie für die entsprechenden ev‐Gene der beiden übrigen Ausgangslinien viel höher lagen. Die Ergebnisse über das Vorkommen von ev‐Genen in diesen Linien mit unterschiedlicher Herkunft bieten insbesondere in Hinsicht auf ev 6 eine einleuchtende Erklärung für die zwischen ihnen beobachteten großen Unterschiede in der Häufigkeit kongenitaler ALV Infektion.

Synergism between the endogenous viral loci ev6 and ev9 in inducing immunological tolerance to avian leukosis virus.

1. The course of infection by exogenous avian leukosis virus was followed in a commercial strain of White Leghorn domestic fowls by measuring viral antigen in feather pulp and egg albumin. Ten days after hatching, 2 out of 360 birds tested positive and at 286 days of age about 60% of the birds had been antigen positive at least once. 2. Among the antigen positive birds, two groups could be distinguished: those which permanently and those which transiently expressed viral antigen. Permanent antigen expression was associated with low antibody titres, while transient antigen expression was associated with high antibody titres. 3. The strain segregated for the two endogenous viral genes ev6 and ev9, both of which express endogenous viral envelope protein, and have been implicated in affecting immune-responsiveness. The antibody titre in individuals positive for both ev6 and ev9, was significantly lower than in those which had none or only one of the two ev-genes. In addition, individuals positive for both ev-genes occurred more frequently in the group permanently positive for viral antigen than in the group transiently antigen positive. 4. The results indicate that there was a strong synergism between ev6 and ev9 in reducing the antibody response to exogenous avian leukosis virus infection, perhaps by inducing immune tolerance or interfering with antibody formation.

Association of the major histocompatibility complex with avian leukosis virus infection in chickens.

1. Association of the B blood group, the major histocompatibility complex (MHC) in chickens, with avian leukosis virus (ALV) infection shown by shedding of group-specific (gs) antigen was studied in an Australorp line selected for short oviposition interval to improve egg production. Three haplotypes (B8a, B9a and B21) were segregating in this line at frequencies of 66.7, 15.6 and 17.8%, respectively, averaged over three generations. 2. The relative risk (odds ratio) of a hen becoming a gs-antigen shedder was calculated for progenies of the dams shedding gs-antigen and those of non-shedding dams separately and pooled over three generations. In the progenies of shedding dams, the relative risk was not significantly different from 1.0 for the three haplotypes. In contrast, in the progenies of non-shedding dams, the relative risk was 0.67, 0.48 and 2.53 for B8a, B9a and B21, respectively, with the last two ratios being significantly different from 1.0. 3. The average effect of haplotype substitution on probability of shedding was estimated from a linear logistic model. The estimates (relative to zero for B8a) for B9a and B21, respectively, were -0.26 and 0.03 among the progenies of shedding dams, and -0.16 and 0.87 among the progenies of non-shedding dams. The last estimate only was highly significant. 4. These results suggest that the three haplotypes were similar in susceptibility to congenital infection through hatching eggs, but differed in susceptibility to post-hatching infection from other infected birds.

The Influence of ev 6 on the Immune Response to Avian Leukosis Virus Infection in Rapid-Feathering Progeny of Slow- and Rapid-Feathering Dams

Endogenous virus (EV) locus ev6 encodes only virus envelope glycoprotein. The influence of ev6 on the immune response to contact infection with hatchmates infected with avian leukosis virus (ALV) was compared in replicate hatches. The ALV Subgroup E-resistant, rapid-feathering (RF) female chickens produced by slow-feathering (SF) and RF dams with and without ev6 were exposed at hatch to hatchmates infected with ALV Subgroup A (Strain RPL-40). The RPL-40 viremia, shedding, and virus neutralizing antibodies were measured among pullets from two hatches at 22 wk of age. Although significant (P less than .05) differences between hatches in the immune response to contact infection were noted among ev6+ pullets, significantly fewer ev6+ pullets seroconverted than their ev6- hatchmates. At 22 wk of age, significantly more lymphomas were also found among ev6+ pullets than among ev6- hatchmates. In flocks wherein both parents and progeny were homozygous resistant to Subgroup E virus, there was no deterimental maternal effect on RF progeny from SF dams that carried ev21. These results also confirm that selection for genetic cellular resistance to Subgroup E ALV infection eliminates congenital transmission of EV21.