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At least 19 recordsLinked to original sources
PubMed1980

Correlation between cell killing and massive second-round superinfection by members of some subgroups of avian leukosis virus.

Avian leukosis viruses of subgroups B, D, and F are cytopathic for chicken cells, whereas viruses of subgroups A, C, and E are not. The amounts of unintegrated linear viral DNA in cells at different times after infection with cytopathic or noncytopathic viruses were determined by hybridization and transfection assays. Shortly after infection, there is a transient accumulation of unintegrated linear viral DNA in cells infected with cytopathic avian leukosis viruses. By 10 days after infection, the majority of this unintegrated viral DNA is not present in the infected cells. The transient cytopathic effect seen in these infected cells also disappears by this time. Low amounts of unintegrated linear viral DNA persist in these cells. Cells infected with noncytopathic viruses do not show this transient accumulation of unintegrated viral DNA. Cells infected with cytopathic viruses and subsequently grown in the presence of neutralizing antibody do not show the transient accumulation of unintegrated viral DNA or cytopathic effects. These results demonstrate a correlation between envelope subgroup, transient accumulation of unintegrated linear viral DNA, and transient cell killing by avian leukosis viruses. The cell killing appears to be the result of massive second-round superinfection by the cytopathic avian leukosis viruses.

Animals↗
PubMed1994

Establishment of interference in osteoblasts by an osteopetrosis-inducing avian leukosis virus.

Avian leukosis virus (ALV)-induced osteopetrosis is characterized by the presence of unintegrated viral DNA is diseased bone. To learn more about this phenomenon, ALVs with high (Br21) and low (RAV-1) osteopetrotic potential have been compared for the ability to establish superinfection resistance in cultures of calvarial-derived osteoblasts. Both viruses could establish interference in osteoblast cultures that were maintained as growing cells. This interference was maintained when cultures were induced to differentiate. These results suggest that the unintegrated viral DNA in osteopetrotic bone is not due to the inability of osteopetrosis-inducing viruses to establish superinfection resistance in osteoblasts.

Animals↗
PubMed1980

Viral DNA in bursal lymphomas induced by avian leukosis viruses.

Avian leukosis viruses (ALV) induce malignant lymphoma of the bursa of Fabricius. Viral DNA in tumors and normal tissues from infected birds were analyzed by using restriction endonucleases. Viral DNA fragments diagnostic of the exogenous ALV were easily detected in tumors, uninvolved bursal tissue, kidney, and erythrocyte nuclei. Exogenous viral DNA was more difficult to detect in liver. Using a restriction endonuclease (SacI) which cleaves linear unintegrated ALV DNA in a single site to define integration sites in DNA from the various tissues, we were able to detect ALV DNA only in tumor tissue. We concluded that the proviral DNA detected in the various nontumor tissue must be integrated in multiple sites. The appearance of ALV integration sites uniquely in tumors suggests that they are clonal growths. Furthermore, the data suggested the presence of a single exogenous integration site for the ALV provirus in each of six early neoplastic bursal nodules. This provirus appeared to retain the organization of EcoRI and BamHI recognition sequences present in the genome of virus used to infect the birds. The ALV integration site appeared different in each of the tumors studied. In a widespread metastatic lymphoma, multiple ALV integration sites were found as well as structural alterations in at least some copies of the ALV provirus.

Animals↗
PubMed1983

Activation of the cellular oncogene c-erbB by LTR insertion: molecular basis for induction of erythroblastosis by avian leukosis virus.

Avian leukosis virus (ALV), a slowly oncogenic retrovirus, induces in chickens a variety of neoplasms, including lymphoid leukosis and erythroblastosis. In lymphoid leukosis, a cellular oncogene, c-myc, is activated by the insertion of ALV LTR. We provide evidence that ALV utilizes a similar mechanism in erythroblastosis induction by activating a different cellular oncogene, c-erbB. We report the isolation, from leukemic erythroblast DNA, of a clone that represents the viral-cell junction fragment and carried the ALV LTR and part of the c-erbB locus. Restriction and sequence analyses reveal that the LTR is located upstream from the erbB coding region and is oriented in the same transcriptional direction; such a structure would be compatible with the promoter-insertion type of activation. Our findings provide a molecular explanation for the multipotency of slowly oncogenic retroviruses.

Animals↗
PubMed1969

Yellow fever vaccine. II. Antigenicity and neurovirulence of a vaccine seed free from avian leukosis virus.

Avian leukosis virus (ALV)-free candidate primary and secondary seed lots were indistinguishable from corresponding ALV-contaminated lots with respect to (i) potency as measured by titration in newborn and weanling mice and in the MA-104 plaque system, (ii) degree of viscerotropism as measured by viremia in monkeys, (iii) neurotropism as determined by the monkey neurovirulence test, and (iv) potency as determined by antibody response in monkeys inoculated by the intracerebral route.

Animals↗
PubMed1997

Rapid induction of B-cell lymphomas by avian leukosis virus.

Avian leukosis viruses (ALVs) that induce rapid B-cell lymphomas integrate into the c-myb gene and produce an ALV-myb read-through RNA, which is spliced to produce a truncated Myb protein. The genetic determinants of such recombinant ALVs have been mapped to a 42-nt deletion within the gag gene. This deletion increases splicing efficiency since it is located within a negative regulator of splicing. We propose that the deletion leads to increased production of Myb protein by increasing splicing of an ALV-myb pre-mRNA.

Animals↗
PubMed2005

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.

Animals↗
PubMed2002

Endocytosis is a critical step in entry of subgroup B avian leukosis viruses.

The avian leukosis virus (ALV) entry mechanism is controversial, with evidence for and against a low-pH requirement for viral fusion. To further address this question, we tested the entry of human immunodeficiency virus type 1 (HIV-1) pseudotyped with the envelope protein of subgroup B ALV (ALV-B) in the presence of three different lysosomotropic agents. These lysosomotropic agents were able to block the entry of wild-type and pseudotyped ALV-B in two different cell lines, strongly suggesting that ALV-B requires a low-pH step for entry. ALV-B and pH-dependent Semliki Forest virus (SFV) entered cells with slower uptake kinetics than HIV-1, which is pH independent. These slow uptake rates support the theory that ALV-B utilizes endocytic pathways to enter cells. Using immunofluorescence and electron microscopy analysis, we visualized the colocalization of virus particles with the endosomal marker transferrin and demonstrated virus particles in clathrin-coated vesicles and endosome-like structures. Surprisingly, a low-pH treatment did not overcome the inhibition of ALV-B entry by lysosomotropic agents. This indicates that, in contrast to SFV, ALV-B is unable to fuse at the cellular surface, even at a low pH. Taken together, our findings suggest that endocytosis and a subsequent low-pH step are critical for successful ALV-B infection.

Ammonium Chloride↗
PubMed2004

Reduced Myc overexpression and normal B-cell differentiation mediate resistance to avian leukosis virus lymphomagenesis.

Avian leukosis virus (ALV) induces bursal lymphoma in tumor-susceptible chicken strains after proviral integration within the c-myc gene, and subsequent expansion of Myc-overexpressing lymphocytes within transformed follicles. Line 6(3) strain chickens are resistant to ALV tumorigenesis, largely failing to develop Myc-transformed follicles, although they show similar levels of ALV infection and integration as lymphoma-susceptible strains. Immunohistochemical analysis determined that the transformed follicles that do arise in lymphoma-resistant birds show much lower and more variable Myc overexpression than those of susceptible birds. This reduced Myc overexpression fails to block B-cell differentiation in resistant birds, while high Myc consistently blocks development at a late embryo stage in susceptible birds. This failure of Myc to block differentiation results in a normal pattern of posthatching bursal emigration in resistant transformed follicles, while transformed follicles of susceptible birds grow rapidly due to blocked emigration. Forced Myc overexpression produces transformed follicles in resistant birds, indicating that resistant lymphocytes can tolerate high Myc expression. The coding sequence and expression of the endogenous c-myc gene is the same in resistant and susceptible birds, suggesting that genetic resistance is instead mediated by reduced ALV LTR enhancer-driven transcription in the target lymphocytes of resistant birds.

Animals↗
PubMed1998

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.

Animals↗
PubMed2002

The feather tips of commercial chickens are a favorable source of DNA for the amplification of Marek's disease virus and avian leukosis virus, subgroup J.

Marek's disease virus (MDV), a herpesvirus, and avian leukosis virus, subgroup J (ALV-J), a retrovirus, are oncogenic viruses of poultry. The present report describes a case-report study aimed at examining the efficacy of amplifying MDV and/or ALV-J from feather-tip DNA as compared with DNA purified from liver and spleen. We show that the polymerase chain reaction for MDV and ALV-J env using DNA from feather tips was more effective for diagnosis of naturally infected commercial chickens than using the liver and spleen.

Animals↗
PubMed2006

Seroprevalence of avian influenza virus, infectious bronchitis virus, reovirus, avian pneumovirus, infectious laryngotracheitis virus, and avian leukosis virus in Nigerian poultry.

Eight poultry farms in Nigeria, including chickens from nine breeder, 14 broiler, 28 pullet, 11 layer, and three cockerel flocks, were tested for antibody seroprevalence to the following poultry viruses of potential economic importance: infectious bronchitis virus (IBV), avian reovirus, avian pneumovirus (APV), infectious laryngotracheitis virus (ILTV), avian influenza virus (AIV), and avian leukosis virus (ALV). Serum samples were collected between 1999 and 2004 and were tested for antibodies using commercial enzyme-linked immunosorbent assay (ELISA) kits. Seroprevalence was very high for IBV (84%); intermediate for reovirus (41%), APV (40%), and ILTV (20%); and very low for ALV (<5%) antibodies. By commercial ELISA, the seroprevalence of antibodies against AIV was, in some flocks, up to 63%. However, more specific assays did not confirm AIV antibodies, indicating that all flocks tested were free of avian influenza antibodies. Birds seemed to be first infected by IBV (at about 7 wk of age), then by reovirus at 12 wk, before they became infected by APV (week 25) and ILTV (week 30). This is the first report of serological evidence of the above viruses in West Africa. Further studies are necessary to assess economic losses due to these avian viruses and the costs and benefits of countermeasures.

Aging↗
PubMed1987

Embryonic infection with the endogenous avian leukosis virus Rous-associated virus-0 alters responses to exogenous avian leukosis virus infection.

We inoculated susceptible chicken embryos with the endogenous avian leukosis virus Rous-associated virus-0 (RAV-0) on day 6 of incubation. At 1 week after hatching, RAV-0-infected and control chickens were inoculated with either RAV-1 or RAV-2, exogenous viruses belonging to subgroups A and B, respectively. The chickens injected with RAV-0 as embryos remained viremic with exogenous virus longer and either failed to develop type-specific humoral immunity to exogenous virus or developed it later than the control chickens not inoculated with RAV-0. The RAV-0-injected chickens also developed neoplasms at a much higher frequency than did the control chickens. We suggest that the lower immune responses of the RAV-0-injected chickens were due to an immunological tolerance to envelope group-specific glycoproteins shared among endogenous and exogenous viruses.

Animals↗
PubMed1978

Comparison of the RNA-dependent DNA polymerase of an endogenous avian leukosis virus to the polymerase of an exogenous avian leukosis virus.

RNA-dependent DNA polymerases from Rous-associated virus-O and avian myeloblastosis virus were partially purified by affinity chromatography and compared to each other. The enzymes are indistinguishable in the immunoglobulin inhibition test and by several enzymological criteria, such as optimum curves for the concentrations of Mg2+, K+, H+; monophasic Lineweaver-Burk plot for dTTP and biphasic Lineweaver-Burk plot for dGTP. In thermal inactivation studies a small difference can be observed, suggesting a minor difference in the physical structures of the enzymes. Our findings are consistent with the idea that the RNA-dpendent DNA polymerases of endogenous and exogenous avian leukosis viruses are very closely related to each other and therefore may be regarded as one group of polymerases.

Antigen-Antibody Reactions↗
PubMed1981

Expression of Forssman antigen of avian lymphoblastoid cell lines transformed by Marek's disease virus or avian leukosis virus.

The expression of Forssman-type heterophile antigen on Marek's disease (MD) virus (MDV)-transformed cell lines, MDCC-MSBI 1, -HP1, -RP1 and -BP1, and avian leukosis virus (ALV)-transformed cell lines, LSCC-1104B1 and -1104X5 was investigated by membrane immunofluorescence and complement-dependent antibody cytotoxicity tests. Forssman antigen was detected on a high percentage of the cells in two ALV-transformed cell lines and on a smaller percentage of splenic lymphocytes from normal chicken. Of the MDV-transformed cell lines tested only the RP1 and BP1 cell lines, derived from transplantable MD tumours, expressed Forssman antigen, while the MSB1 and HP1 cell lines, derived from MD lymphomas, did not. Forssman antigen appears to be unrelated to MD tumour-associated surface antigen (MATSA).

Animals↗
PubMed2001

Heterophil function and resistance to staphylococcal challenge in broiler chickens naturally infected with avian leukosis virus subgroup J.

Avian leukosis virus subgroup J has a high tropism for myeloid lineage cells and frequently induces neoplastic transformation of myelocytes. The impact of congenital avian leukosis virus subgroup J infection on the function of circulating heterophils and susceptibility to staphylococcal infection was investigated. Six-week-old broiler chickens negative for exogenous avian leukosis viruses or congenitally infected with avian leukosis virus subgroup J were inoculated intravenously with 10(6) colony-forming units of Staphylococcus aureus, and pre- and postinoculation heterophil function was assessed. All chickens developed a leukocytosis with heterophilia after inoculation, but total leukocyte and heterophil counts were significantly higher in leukosis-negative chickens than in virus-infected chickens. Tenosynovitis was more severe in leukosis-negative chickens, and 2/10 (20%) of the virus-infected chickens had no histologic evidence of tenosynovitis. Osteomyelitis in the tibiotarsus or tarsometatarsus developed in 5/10 (50%) of the chickens in each group. S. aureus was recovered from the hock joint of 6/10 (60%) of the chickens in each group. Heterophils from all chickens exhibited similar phagocytic ability pre- and postinoculation. Heterophils from virus-infected chickens exhibited less bactericidal ability preinoculation than did heterophils from leukosis-negative chickens. However, postinoculation bactericidal ability was similar in both groups. Avian leukosis virus subgroup J provirus was present in heterophils isolated from congenitally infected chickens. Heterophils isolated from broiler chickens congenitally infected with avian leukosis virus subgroup J exhibit no significant functional deficits, and infected and uninfected chickens exhibit similar susceptibility to staphylococcal infection.

Animals↗