Age related resistance to avian leukosis virus. III. Infectious virus, neutralising antibody and tumours in chickens inoculated at various ages

Viraemia and neutralising antibodies were determined in chickens of six age-groups following inoculation with leukosis virus of subgroups A and B at the age of 1 day, and 2, 4, 6, 8 and 10 weeks respectively. The birds were kept in a filtered air positive pressure (FAPP) house. A seventh age-group, accommodated in a separate FAPP-house, was used as an untreated control. Serum samples, received at biweekly intervals between 1-17 weeks post-inoculation, from birds of the groups inoculated at 4, 6, 8 and 10 weeks of age, showed at 1 week post-inoculation a transient viraemia followed by neutralising antibodies at the later sampling times. Neutralising antibody to subgroup A virus was detected in nearly all birds tested; this was not so for antibody to subgroup B. In all four groups the average titre of the former antibody was higher than that of the latter. Midway through the laying period birds of each group inoculated with leukosis virus, and some of the uninoculated controls, were challenged by infection with either subgroup A or B virus. At termination of the experiment survivors from each group were tested for the presence of leukosis virus. The virus recovery was performed with plasma samples, white blood cell preparations and explant cultures of various organs. The plasma samples were all negative; the great majority of blood cell specimens received from birds inoculated early with leukosis virus were positive, whereas the majority of the preparations from the birds inoculated later remained negative. The organ explants from the two youngest age groups were mostly leukosis virus-positive, from the birds inoculated at 4 weeks of age the spleen and kidney explants contained leukosis virus whereas in the groups inoculated at 6, 8 and 10 weeks of age only the spleen explants of birds challenged with subgroup A virus In a subsidiary experiment, started 4 months after the challenge infection, four birds from each group (two challenged with leukosis virus of subgroup A and two with subgroup B) were accommodated in isolators. The birds were challenged again, this time with Rous sarcoma virus (RSV) of the homologous subgroup used for the previous challenge. The tests for virus just prior to the challenge showed leukosis virus only in the white blood cell preparations from the birds in the three youngest age groups; the birds from the older groups were virus-negative. The serological tests after challenge showed neutralising antibodies to both subgroups in birds of nearly all groups. Tumour formation at the site of injection was mainly observed in the chickens challenged with RSV of subgroup B. The virological and serological results as well as the tumour response show that the immune system of birds between 0-4 weeks of age is insufficiently developed to cope with a controlled exposure with leukosis virus, whereas in birds of 4-10 weeks of age an adequate immunological response has developed. The significance of the presence of leukosis virus in sera, plasma, white blood cell preparations and organ explant cultures is mentioned. In programmes for the control of lymphoid leukosis in reproductive stock the use of information on virus and neutralising antibodies is recommended.     

Effects of age at infection with serotype 2 Marek's disease virus on enhancement of avian leukosis virus-induced lymphomas

Inoculation of susceptible, 15I(5x)7(1) chickens with serotype 2 Marek's disease virus (MDV) at various ages had no influence on the development of avian leukosis virus (ALV)-induced viraemia or antibody in chickens infected with ALV and turkey herpesvirus (HVT) at hatch. However, the incidence of ALV-induced lymphoma (LL) was significantly higher in chickens infected with ALV and HVT at hatch and inoculated with serotype 2 MDV up to 6 weeks of age than in chickens receiving serotype 2 MDV at 8 to 10 weeks, uninoculated chickens, or chickens inoculated only with HVT. Metastatic LL in the viscera was more frequently observed in chickens inoculated with serotype 2 MDV at hatch and 2 weeks than in chickens inoculated at 6 weeks of age. In another experiment, chickens inoculated with serotype 2 MDV and HVT at hatch and infected with ALV at 2 or 4 weeks of age developed significantly higher incidence of LL than in uninoculated chickens or chickens inoculated only with HVT. The data suggest that enhancement of LL can occur in chickens infected with serotype 2 MDV within 6 weeks after infection with ALV at hatch. The data also suggest that infection of chickens with serotype 2 MDV at hatch may increase the rate of metastasis of LL and may interfere with age resistance to development of LL.     

Horizontal transmission of lymphoid leukosis virus. Influence of age, maternal antibodies and degree of contact exposure

Eight groups of 1-day-old or 8-week-old chickens were exposed by contact to lymphoid leukosis virus (LLV) infection. Five groups of about 60 spf chickens were used. Three groups of the same size were progeny from LLV vaccinated hens. Five groups were housed in one chicken house in close contact with a large number of immunologically tolerant chickens (virus "spreaders"). On two occasions infectious LLV was recovered from air/dust samples collected in this house. In the second house a small number of congenitally infected birds generated a mild degree of LLV exposure. It was demonstrated that infection by contact may lead to lymphoma formation and congenital virus transmission. The incidence of virus infection and LL mortality in the groups of birds exposed at 8 weeks of age were significantly lower than in chickens exposed at 1 day of age. In addition, about 100-fold differences in numbers of LLV-associated white blood cells were observed between both age groups. These results indicate that in addition to resistance to tumour formation, resistance to LLV infection develops in the chicken with increasing age. Maternal antibodies, present in three groups exposed at 1 day of age, reduced the rate of infection and the incidence of LL.     

Infectious bursal agent of chickens reduces the incidence of lymphoid leukosis

In tests to determine whether infectious bursal agent (IBA) would significantly affect the incidence of lymphoid leukosis (LL), chickens were inoculated with an LL virus and subsequently exposed to IBA at 2 weeks or 8 weeks of age. When chickens were exposed to IBA at either age, the IBA significantly reduced the incidence of LL without affecting the chicken's ability to produce antibody to sheep erythrocytes. IBA probably destroys the target cells necessary for the development of LL tumours. It is postulated that IBA may play a role in the field incidence of LL.     

Age‐related resistance to Avian Leukosis virus I. Influence of age at exposure on mortality and congenital transmission

Groups of White Leghorn chickens were inoculated at 1 day and at 2, 4, 6 and 8 weeks of age respectively with a mixture of leukosis viruses of subgroups A and B. The five infected groups were kept in a filtered air positive pressure house. A sixth group was accommodated separately in a similar house as a control.

All birds which died or were removed were subjected to pathohistological examination; diagnosis of lymphoid leukosis was made upon either gross lesions plus microscopical lesions or microscopical lesions only.

The incidence of lymphoid leukosis in the infected groups appeared inversely proportional to age of infection, i.e. the mortality due to lymphoid leukosis decreased from 54.3% in the group infected at 1‐day‐old to 7.4% in the group infected at 8 weeks of age. Prevalence of leukosis in the latter group may be attributed to a small number of chicks already infected vertically with the virus.

Congenital transmission of leukosis virus was demonstrated in embyros in the groups infected at 1‐day‐old, 2, 4 and 6 weeks of age. In the latter group congenital transmission was extremely low; from 214 pooled embryo extracts (1007 embryos) only 2 (0.9%) contained leukosis virus. In the group infected at 8 weeks of age no virus was detected in the embryos. Congenital transmission of leukosis virus appeared to be related to age of infection, i.e. early infection went parallel with a high rate of transmission. The pattern of congenital transmission was erratic and the number of hens shedding leukosis virus continually was small.

From the results in this trial it is concluded that both lymphoid leukosis and congenital transmission occur rarely if chickens (born free of leukosis virus) are kept free from infection during the first 6–8 weeks of life and subsequently are injected with a relatively high dose of leukosis virus.     

Variation in tolerance induction and oncogenicity due to strain of avian leukosis virus

Chickens were inoculated as embryos or orally at hatching with various doses of four strains of avian leukosis virus (ALV) subgroup A (RAV-1, RPL40, RPL41 and RPL42). Viraemia, antibody and tumours in chickens of various groups were compared; ALV shedding was determined, but only in chickens inoculated with virus at hatching. Results indicate that 95% to 100% of chickens embryonally inoculated with 105 infectious units of virus were viraemic at hatching, regardless of the strain of virus used. However, the incidence of viraemia in groups of chickens embryonally inoculated with 100 infectious units of virus varied, depending on the strain of virus, from 5% to 72%. All embryonally inoculated chickens, that had detectable virus at hatching and survived to 16 weeks of age were immunologically tolerant to the virus. ALV-induced tumours ranged from 4% to 47% depending on the strain of virus. Chickens inoculated orally at hatching did not develop immuno-logical tolerance to the virus; 13% to 76% of these chickens, depending on the strain of virus, had antibody by 18 weeks of age. ALV shedding in albumen of eggs or cloacal swabs at 42 weeks of age varied from 7% to 9%. Data from this study indicate that the strain of ALV may influence induction of immunological tolerance and tumours in embryonally inoculated chickens and induction of antibody in nontolerantly infected chickens. The data also suggest that chickens that are viraemic at hatching are probably incapable of breaking tolerance and developing antibody.     

Further observations on serotype 2 Marek's disease virus-induced enhancement of spontaneous avian leukosis virus-like bursal lymphomas in ALVA6 transgenic chickens

Breeders of the 2009 generation of Avian Disease and Oncology Laboratory transgenic chicken line ALVA6, known to be resistant to infection with subgroups A and E avian leukosis virus (ALV), were vaccinated at hatch with a trivalent Marek's disease (MD) vaccine containing serotypes 1, 2, and 3 Marek's disease virus (MDV) and were maintained under pathogen-free conditions from the day of hatch until 75 weeks of age. Spontaneous ALV-like bursal lymphomas, also termed lymphoid leukosis (LL)-like lymphomas, were detected in 7% of the ALVA6 breeders. There was no evidence of infection with exogenous and endogenous ALV as determined by virus isolation tests of plasma and tumour tissue homogenates. For the next three generations, serotype 2 MDV was eliminated from the trivalent MD vaccine used. Results show, for the first time, that removal of serotype 2 MDV from MD vaccines eliminated spontaneous LL-like lymphomas within 50 to 72 weeks of age for at least three consecutive generations. Two experiments were also conducted to determine the influence of in ovo vaccination with serotype 2 MD vaccines on enhancement of spontaneous LL-like lymphomas in ALVA6 chickens. Chickens from the 2012 generation were each inoculated in ovo or at hatch with 5000 plaque-forming units of serotype 2 MDV. Results indicate that by 50 weeks of age the incidence of spontaneous LL-like lymphomas in chickens inoculated in ovo with serotype 2 MDV was comparable with that in chickens inoculated with virus at hatch, suggesting that the augmentation effect of serotype 2 MDV is independent of age of vaccination.     

Response of meat-type chickens to infection with RAV-1 avian leukosis virus

Meat-type and White Leghorn chickens were inoculated with the RAV-1 strain of avian leukosis virus at 1 day of age and the severity of infection was assessed by clinical illness, haematology and post-mortem findings. The following were examined from selected birds: histological section for chronic mononuclear myocarditis, immunohistochemically-stained sections of myocardium, spleen, bursa of Fabricius and kidney for group-specific viral antigen, and ultrathin sections of these tissues for virus particles by electron microscopy. The experiment was terminated at 115-122 days. Approximately one-third of the 52 inoculated White Leghorns appeared anaemic at 3-4 weeks of age whereas there was no evidence of anaemia in 177 inoculated meat-type birds or in uninoculated birds of either type. Haemograms confirmed these observations. The first tumour found was a myelocytoma and it was in a meat-type bird at 65 days. Of the 151 meat-type birds of the inoculated group alive at 65 days, 8.5% developed nephroblastomas, but there were no cases of lymphoid leukosis. Myocarditis and virus replication in myocardium were usually more extensive in chickens that developed nephroblastomas than in those without such lesions. In 17 uninoculated control chickens examined between 26 and 122 days of age there were no virus particles or lesions in myocardium.     

Reduction of horizontal transmission of avian leukosis virus subgroup J in broiler breeder chickens hatched and reared in small groups

Transmission of avian leukosis virus, subgroup J (ALV-J), from donor chickens inoculated as embryos to simulate congenital infection to uninfected hatchmates was studied in two strains of commercial broiler breeder chickens. Chicks of two commercial lines free of ALV-J became infected when hatched (1/2 lots positive) or reared (8/8 lots positive) in direct physical contact with ALV-J-infected donors. Infection also occurred when chicks were exposed in the hatchery to ALV-J-infected donors by cloacal swab transfer (2/2 lots positive), needle transfer during subcutaneous inoculation (2/2 lots positive), or ingestion of infected meconium (2/2 lots positive). However, transmission was delayed or prevented by wire partitions in the hatcher and rearing of small groups in cubicles, and rarely (1/10 lots positive) resulted from short-term direct or indirect contact. In a simulated field test, a flock of 503 broiler breeder chickens with an initial embryo infection rate of 4.6% was hatched and reared as 48 small groups to 4 weeks of age. Groups were tested at hatch and at 3 weeks, and 14 infected groups were eliminated. This flock tested negative for ALV-J infection from 4 to 32 weeks and did not transmit infection to progeny or develop tumours. A control group of 377 chickens with a similar initial infection rate was hatched and reared as a single group. This control flock transmitted virus to 5.7% of its progeny and about 5% of the hens developed tumours. The small-group hatching and rearing practices employed in these studies allowed for the accurate identification and removal of groups containing chickens infected prior to hatching and prevented horizontal transmission of ALV-J between uninfected and infected groups for at least 4 weeks. More importantly, application of these procedures successfully eradicated ALV-J in a single generation under laboratory conditions. This suggests that similar procedures could be a valuable adjunct to virus eradication programmes in the field.     

An outbreak of lymphomas in commercial broiler breeder chickens vaccinated with a fowlpox vaccine contaminated with reticuloendotheliosis virus

Gross and microscopic examinations of affected tissues from chickens of two commercial broiler breeder flocks aged 27 and 31 weeks revealed lesions of visceral lymphomas with bursal involvement in some chickens. Reticuloendotheliosis virus (REV), but not avian leukosis virus (ALV), was isolated from blood of affected chickens. Furthermore, DNA extracted from tumours tested positive for REV, but not for ALV or Marek's disease virus by polymerase chain reaction (PCR) test. Attempts to determine the source of REV infection included testing a commercial fowlpox (FP) vaccine used to immunize flocks at 7 days of age. Chicken-embryo fibroblasts inoculated with the FP vaccine tested positive for REV by PCR and immunofluorescent tests. REV was also isolated from plasma of pathogen-free chickens experimentally inoculated with FP vaccine at hatch; two of eight (25%) inoculated chickens developed lymphomas by 34 weeks of age. Antigenic characterization of REV isolated from commercial broiler breeder chickens and from FP vaccine, using monoclonal antibodies, revealed that both isolates belong to subtype 3 of REV. The data represent the first report of an outbreak of REV-induced lymphomas in commercial chickens. The data also indicate that the source of REV infection is an REV-contaminated commercial FP vaccine.     

Generation and infectivity titration of an infectious stock of avian hepatitis E virus (HEV) in chickens and cross-species infection of turkeys with avian HEV

Avian hepatitis E virus (HEV), a novel virus identified from chickens with hepatitis-splenomegaly syndrome in the United States, is genetically and antigenically related to human HEV. In order to further characterize avian HEV, an infectious viral stock with a known infectious titer must be generated, as HEV cannot be propagated in vitro. Bile and feces collected from specific-pathogen-free (SPF) chickens experimentally infected with avian HEV were used to prepare an avian HEV infectious stock as a 10% suspension of positive fecal and bile samples in phosphate-buffered saline. The infectivity titer of this infectious stock was determined by inoculating 1-week-old SPF chickens intravenously with 200 microl of each of serial 10-fold dilutions (10(-2) to 10(-6)) of the avian HEV stock (two chickens were inoculated with each dilution). All chickens inoculated with the 10(-2) to 10(-4) dilutions of the infectious stock and one of the two chickens inoculated with the 10(-5) dilution, but neither of the chickens inoculated with the 10(-6) dilution, became seropositive for anti-avian HEV antibody at 4 weeks postinoculation (wpi). Two serologically negative contact control chickens housed together with chickens inoculated with the 10(-2) dilution also seroconverted at 8 wpi. Viremia and shedding of virus in feces were variable in chickens inoculated with the 10(-2) to 10(-5) dilutions but were not detectable in those inoculated with the 10(-6) dilution. The infectivity titer of the infectious avian HEV stock was determined to be 5 x 10(5) 50% chicken infectious doses (CID(50)) per ml. Eight 1-week-old turkeys were intravenously inoculated with 10(5) CID(50) of avian HEV, and another group of nine turkeys were not inoculated and were used as controls. The inoculated turkeys seroconverted at 4 to 8 wpi. In the inoculated turkeys, viremia was detected at 2 to 6 wpi and shedding of virus in feces was detected at 4 to 7 wpi. A serologically negative contact control turkey housed together with the inoculated ones also became infected through direct contact. This is the first demonstration of cross-species infection by avian HEV.     

Studies on experimental tenosynovitis in light hybrid chickens

A group of light hybrid chicks was inoculated via the footpad at 1-day-old with an avian reovirus isolated from ruptured gastrocnemius tendons, and were housed with a similar number of uninoculated chicks (in-contacts) from the same hatch. Though all inoculated birds showed swellings of the injected leg after 7 days, lesions of tenosynovitis did not develop in the other leg or in either leg of in-contacts until they were 6- to 7-weeks-old. Lesions in leg tendons, and particularly the digital flexors, persisted in both inoculated and in-contact birds until the termination of the experiment at 33 weeks of age. Reovirus was recovered for varying periods from the trachea, intestine, hock and footpad of inoculated chickens commencing 1 week after infection, and from the same tissues of in-contacts but from 2 weeks, and generally for shorter periods. In both groups virus persisted for at least 13 weeks in the hock joint or surrounding tissues and cloacal swabs were positive between the 14th and 16th weeks after inoculation. Fluorescent antibody staining demonstrated penetration of the virus into the tendons. Precipitating antibodies to the reovirus were detectable in both groups between the 3rd and 24th weeks after infection.     

Comparison of complement fixation and phenotypic mixing tests for the detection of lymphoid leukosis virus in egg albumen and embryos of individual eggs

Individual eggs, collected from 14 hens over a period of 10 weeks, were tested for lymphoid leukosis (LL) virus by four methods. The chickens were selected from a conventional flock on the basis of virus recovery from embryos 3 months earlier. Albumen samples and extracts of embryos were examined by complement fixation (CFT) and phenotypic mixing tests (PMT). Most eggs positive for LL virus (LLV) and/or group specific (gs)-antigen were detected by testing of embryo extracts by PMT and CFT. Examination of albumens yielded less LLV and gs-antigen positive eggs. However, because a few birds produced eggs with predominantly gs-antigen in the albumen and less frequently with virus in the embryos from the same eggs, the combination of CFT on both albumen and embryo extract proved to be the most sensitive detection system. CFT on both albumen and embryo are easier to perform than PM tests and therefore may be useful in LL eradication programmes. The majority of the hens intermittently transmitted virus and/or gs-antigen to embryos. The results of this study indicate that congenital transmission patterns of LLV infections may be different in individual birds.     

Responses of isolator-derived Japanese quail and quail cell cultures to selected animal viruses.

Thirteen oncogenic and necrotizing animal viruses were assayed in LIFE Sciences, Inc. (LSI)-specific pathogen-free Japanese quail and LSI-specific pathogen-free chicken embryo cell cultures. Nine viruses produced similar titers in the quail and chicken cell systems, whereas four viruses showed significantly higher titers in chickens. Young Japanese quail and chickens were inoculated with five selected avain viruses and maintained in stainless-steel isolators. Comparable responses were noted in quail and chickens injected with Newcastle disease virus and avain leukosis virus, but quail were significantly more resistant than chickens to fowl pox virus, laryngotracheitis virus, and Marek's disease herpesvirus. Although no overt symptoms of disease were observed in Japanese quail inoculated with most avain viruses, neutralizing antibody or virus was detected, indicating presence of an inapparent infection. In one experiment, neutralizing antibody was detected in a comparable number of quail and chickens after inoculation with avian leukosis virus. Avian leukosis virus viremia was observed at 12 and 70 days postinoculation, with the COFAL (complement fixation for avian leukosis) titers similar for quail and chickens. Most quail infected with Marek's disease herpesvirus produced neutralizing antibody within 70 days but showed no classical symptoms of Marek's disease even when held for 5 months. In contrast, all chickens inoculated with Marek's disease herpesvirus died within 20 days. The utility of quail embryo cell cultured in the preparation of vaccines and biological reagents is discussed.     

Myocardial cytoplasmic inclusions in chickens with haemangioma and lymphoid leukosis

Twelve of 23 adult chickens (23 to 28 weeks old) affected naturally with haemangioma and lymphoid leukosis (LL) had basophilic cytoplasmic inclusions in myocardial cells. The inclusions were oval, elongated, round or pleomorphic in shape and were rich in RNA. Electron microscopy revealed that the inclusions comprised of electron-dense small granules and doughnut-shaped particles. The significance of inclusions in LL virus infections and LL virus-induced tumours is discussed.     

Experimental infection of chickens with an Australian strain of reticuloendotheliosis virus. 2. Serological responses and pathogenesis

Fifteen SPF chickens were inoculated with an Australian strain of reticuloendotheliosis virus (REV) at 1 day of age and five uninoculated chickens were readily infected by horizontal spread from this group. Antibody detectable by the immunofluorescent antibody (IFA) test developed 3 to 6 weeks after infection, and usually persisted for 20-35 weeks, with maximum titres (40-1280) at 8 to 13 weeks. Agar gel precipitin (AGP) reactions developed more slowly and were variable in duration, the highest proportion of positive reactions being detectable 8 to 13 weeks after infection and persisting for 8 to 30 weeks. Infectious REV was readily detected in the plasma and serum of inoculated chickens 6 weeks after infection and a non-infectious REV antigenaemia usually persisted for at least a further 7 weeks, in the presence or absence of antibody. Development of a detectable REV viraemia was strongly associated with poor body development and premature mortality among the inoculated chickens. In two inoculated chickens which failed to develop detectable serological reactions, a REV viraemia occurred which persisted throughout life. At autopsy, REV was re-isolated from the kidneys of most of the inoculated chickens and from the reproductive and intestinal systems of two birds 22 and 56 weeks after infection.     

A study of vaccination against Marek's disease with an attenuated Marek's disease virus

Approximately 2,000 day-old white leghorn chickens were distributed into 10 pens and half the pens vaccinated with the attenuated strain of HPRS-16. At 72 weeks of age, mortality from non-specific death and Marek's disease was 17.6% and 15.6% respectively, in vaccinated chickens compared with 14.2% and 51.7% in unvaccinated chickens. Body weights of vaccinated chickens were 5.6% higher at 8 weeks of age than unvaccinated chickens. Vaccinated chickens consumed 2.3% more feed and the hen housed egg production and hen day egg production were 58.7% and 7.0% greater than unvaccinated chickens. Vaccination resulted in a 3.8 fold increase in net margin over food and bird costs per bird housed at 16 weeks. Active antibody production to 'A' antigen occurred later and in a smaller proportion of vaccinated chickens than unvaccinated chickens. Viraemia due to vaccination was detected at 2 weeks of age and viraemia due to field virus was detected at 5 weeks of age. The incidence and titres of viraemia due to field virus were higher in unvaccinated chickens compared with vaccinated chickens. No evidence of spread of vaccine virus to unvaccinated chickens could be found. Acute, classical and apathogenic strains of field virus were isolated from vaccinated chickens and strains of field virus were found to persist throughout the life of the vaccinated chickens. Mild classical and/or apathogenic strains were first apparent at 18 weeks of age and increased in proportion thereafter, forming the majority of isolates from 52 weeks of age. Data on individual birds suggested a direct relationship between virus titre and lesion (or Marek's disease) frequency.     

Oncogenicity of avian leukosis viruses of different subgroups and of mutants of sarcoma viruses.

Leukosis viruses of seven subgroups were tested for oncogenicity in chickens susceptible to virus infection and to development of lymphoid leukosis (LL) tumors. All subgroup A viruses and the subgroup B virus tested produced a high incidence of LL and other related neoplasms. Viruses of subgroup C and RAV-61 of subgroup F produced a low level of LL. The RAV-50 of subgroup D produced osteopetrosis. In these tests, the viruses of subgroup E and G and one virus of subgroup F were not pathogenic, possibly because infection was not established in the chickens, the chickens were not susceptible to tumor development by these viruses, or the viruses lacked oncogenicity. All temperature-sensitive mutants of Rous sarcoma virus produced sarcomas, but the level varied. One nontransforming mutant produced sarcomas, and the other three tested produced LL. All three mutants that cause cells to grow as colonies in agar produced a high incidence of sarcomas. Thus, sarcoma viruses, by back-mutation, may lose the ability to transform cells in vitro, to make cells grow in agar colonies, or to induce sarcomas in vivo, yet they retain the ability to produce LL. Conversely, it was previously shown that leukosis viruses may be changed into viruses that transform cells in vitro and produce sarcomas in vivo by suitable passage in chicks.     

Induction of angiosarcomas by ring-necked pheasant virus

Ring-necked pheasant virus, an avian leukosis virus, when injected into 10-day old chick embryos, caused angiosarcomas in the lungs of infected chickens within a short time. Angiosarcomas appeared as localized foci of proliferating cells in the lungs as early as 2 weeks posthatch, and by 6 weeks, the lungs of the infected chickens were frequently filled with tumor cells. Between 3 and 10 weeks of age, 80% of infected chickens died of the angiosarcomas; the 20% which lived 8 weeks or longer had small lung lesions and also developed fibrosarcomas, osteopetrosis, nephroblastoma, and lymphoid leukosis. Chickens with lung tumors were cyanotic, had breathing difficulty, and had packed cell volumes in excess of 50%. Other changes not necessarily correlated with lung tumor mass were stunting, lymphoid organ involution, and profuse diarrhea. Ring-necked pheasant virus has a genome RNA of 8.2 kb. This observation, together with its replication and disease induction after repeated plaque purification, suggests that ring-necked pheasant virus is a replication-competent avian retrovirus. Therefore, our results suggest that ring-necked pheasant virus is an avian leukosis virus which causes angiosarcomas rapidly at high incidence and which, therefore, may induce this type of tumor by a mechanism different from the induction of sarcomas by avian sarcoma viruses.     

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.