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PubMed1983

Specificity in the immunosuppression induced by avian reticuloendotheliosis virus.

Several parameters of the cellular and humoral immune responses of chickens infected with reticuloendotheliosis virus (REV-T), an avian defective acute leukemia virus, or with its helper virus, reticuloendotheliosis-associated virus (REV-A), were evaluated. Spleen cells from chickens infected with REV-T (REV-A) or REV-A exhibited depressed mixed lymphocyte and mitogen responses in vitro. Allograft rejection was delayed by 6 to 14 days in birds infected with REV-A. The specific antitumor cell immune response was also studied by a 51Cr-release cytotoxicity assay. Lymphocytes from chickens infected with low numbers of the REV-T-transformed cells exhibited significant levels of cytolytic reactivity against the 51Cr-labeled REV-T tumor cells in vitro. The mitogen response of lymphocytes from these injected birds was similar to that of uninjected chickens. In contrast, lymphocytes from chickens injected with higher numbers of REV-T-transformed cells exhibited suppressed mitogen reactivity and failed to develop detectable levels of cytotoxic activity directed against the REV-T tumor cells. These results suggest that the general depression of cellular immune competence which occurs during REV-T (REV-A) infection could contribute to the development of this acute leukemia by inhibiting the proliferation of cytotoxic cells directed against the tumor cell antigens. The cytotoxic effect observed after the injection of chickens with non-immunosuppressive levels of REV-T-transformed cells appears to be specific for the REV-T tumor cell antigens since cells transformed by Marek's disease virus or avian erythroblastosis virus were not lysed. In marked contrast, birds whose cellular immune responses were suppressed by infection with REV-A were capable of producing a humoral immune response to viral antigens. Detectable levels of viral antibody, however, did not appear until 12 to 15 days after REV-A infection. Since REV-T (REV-A) induced an acute leukemia resulting in death within 7 to 14 days, it appears unlikely that the ability of chickens to make antiviral antibody influences the development of lethal reticuloendotheliosis.

Animals↗

PubMed1979

Avian reticuloendotheliosis viruses: evolutionary linkage with mammalian type C retroviruses.

Reticuloendotheliosis viruses have been shown to be causative of tumors in a variety of avian species. The major structural protein of these non-genetically transmitted viruses is demonstrated to possess antigenic determinants common to those of all known mammalian type C viruses. These findings establish a mammalian origin for this oncogenic avian retrovirus group. None of the known mammalian type C virus groups demonstrated a closer immunological relationship to avian reticuloendotheliosis viruses. These results suggest that reticuloendotheliosis viruses have been non-genetically transmitted for a long period of evolution or that these viruses may have arisen by relatively recent infection of birds with an as yet undiscovered mammalian type C retrovirus.

Antigens, Viral↗

PubMed1985

In vitro transcription analysis of the viral promoter involved in c-myc activation in chicken B lymphomas: detection and mapping of two RNA initiation sites within the reticuloendotheliosis virus long terminal repeat.

Chicken syncytial virus, a member of the reticuloendotheliosis virus family, induces B-cell lymphomas in chickens that arise by transcriptional activation of the chicken c-myc gene. In vitro transcription studies on cloned tumor DNA containing a deleted chicken syncytial virus provirus integrated upstream from, and in the same transcriptional orientation as, the chicken c-myc coding region were utilized to map possible transcriptional promoters and initiation sites. In vitro transcripts extending into c-myc sequences were initiated at two sites within the downstream long terminal repeat (LTR) closest to c-myc coding sequences. Both initiation sites have been precisely mapped by S1 nuclease and DNA sequencing methods. One site (I1) lies at the U3-R junction of the LTR, and the other site (I2) lies approximately 160 nucleotides upstream. Transcriptional control signals, including TATA- and CAAT-like sequences are present at appropriate distances upstream from the initiation sites. Both initiation sites are utilized to a similar extent. The upstream chicken syncytial virus LTR was also shown to be transcriptionally active in vitro. Two strong transcriptional initiation sites were also found in the LTR of spleen necrosis virus, a related member of the reticuloendotheliosis virus family; therefore, it seems likely that the existence of two transcriptional initiation sites is a common feature of the reticuloendotheliosis virus LTR, in contrast to other previously studied retroviral LTRs that exhibit one such site. The possible implications of these findings are discussed.

Animals↗

PubMed1989

Acquisition of new proviral copies in avian lymphoid cells transformed by reticuloendotheliosis virus.

The expression of the v-rel oncogene of avian reticuloendotheliosis virus (REV-T) transforms and immortalizes very immature avian lymphoid cells. In REV-T-transformed lymphoid cells which were persistently infected with reticuloendotheliosis-associated virus (REV-A), the REV-T proviral copy number increases after the initial integration event. In 23 independently derived REV-T-transformed cell lines, 15 of the 18 virus-producing cell lines had acquired additional proviruses. The rate at which the newly acquired proviral sequences accumulated differed for various cell lines. In some cell lines, additional REV-T proviral copies could be detected as early as 8 months after the initial integration event. A correlation exists between the number of REV-T proviral sequences and the length of time which a given cell line had been propagated in culture. The integration sites occupied by the newly acquired REV-T proviruses were distinct. In contrast, reticuloendotheliosis-associated virus proviral sequences in these REV-T-transformed virus-producing lymphoid cells did not increase during in vitro culture. Furthermore, the acquisition of additional REV-T proviral sequences did not occur in non-virus-producing cell lines. Two of the newly acquired proviral sequences were molecularly cloned and analyzed by restriction endonuclease mapping. Although the newly acquired REV-T proviruses have not sustained major deletions, the viral sequences and the v-rel oncogene display numerous restriction enzyme polymorphisms. The cellular flanking sequences of two newly acquired REV-T proviruses analyzed were unique and shared no homology with flanking sequences of the other REV-T proviruses in these transformed cells. The nucleotide sequence of the virus-cellular DNA junctions of one newly acquired provirus and its cellular sequence prior to proviral integration were defined. A 5-base-pair direct repeat of cellular origin was present on each side of the long terminal repeat, indicating that the mechanism of acquisition of additional REV-T proviral sequences used reverse transcription and integration of new REV-T proviral copies.

Animals↗

PubMed2000

Neoplastic diseases: Marek's disease, avian leukosis and reticuloendotheliosis.

The commercially important neoplastic diseases of poultry are Marek's disease, which is caused by a herpesvirus, and the avian leukoses and reticuloendotheliosis, which are caused by retroviruses. These diseases are responsible for economic loss due to both mortality and depressed performance. Marek's disease virus (MDV) and avian leukosis viruses (ALVs) are prevalent throughout the world, and new strains which arise in particular locations may spread across borders, thereby undermining national disease control measures. Reticuloendotheliosis virus (REV) is also present in many countries. Marek's disease virus is transmitted horizontally only, and international spread in hatching eggs and day-old chicks can be prevented by appropriate hygiene precautions. Transmission of ALV and REV occurs both horizontally and vertically (through the egg), and measures to prevent international spread are more demanding. Marek's disease is controlled by vaccination, whilst avian leukosis is controlled by virus eradication programmes, mainly at the primary breeding level. Similar virus control measures can be applied for reticuloendotheliosis if necessary. No strong evidence exists to suggest that these avian tumour viruses constitute a danger to public health.

Animals↗

PubMed1990

Reticuloendotheliosis virus REV-T(REV-A)-induced neoplasia: development of tumors within the T-lymphoid and myeloid lineages.

Infection of 1-day-old chicks with reticuloendotheliosis virus strain T induces a neoplastic disease that kills the chicks 7 to 14 days postinfection. In association with reticuloendotheliosis-associated virus (REV-A), reticuloendotheliosis virus T (REV-T) induces tumors that are predominantly immunoglobulin M (IgM) negative. We examined a variety of REV-T(REV-A)-induced tumors and tumor-derived cell lines and concluded that the principal IgM-negative tumors that develop in REV-T(REV-A)-infected chicks are neither pre-B or pre-B-pre-T but rather mature T lymphoid and myeloid. Without exception, the immunoglobulin heavy- and light-chain loci were in germ line configuration. Furthermore, the cell lines expressed neither sterile transcripts of the heavy- or light-chain immunoglobulin genes nor elevated levels of c-myb, two characteristics associated with murine pre-B lymphomas. Cell lines were also examined by using monoclonal antibodies for expression of a variety of cell surface markers expressed on B lymphocytes and/or T lymphocytes and/or myeloid cells. These reagents defined two types of IgM-negative tumor cell lines, one CIa+ CT-3+ (T lymphoid) and the other CIa+ CT-3-. By using the same approaches, tumor development was examined following REV-T(REV-A) infection at 1 and 3 weeks post-hatching of cyclophosphamide-treated chicks shown to be devoid of B-lymphoid cells. Again, the tumors that developed were either CIa+ CT-3+ (T lymphoid) or CIa+ CT-3-. Furthermore, the frequency and rate with which IgM-negative tumors developed in cyclophosphamide-treated chicks were not different from those observed in normal chicks. In 3-week-old cyclophosphamide-treated chicks, the presence of CIa+ CT-3- tumors bearing hematopoietic lineage markers, such as CLA-3 and 5M19, are most likely to have been derived from cells within the myeloid lineage.

Animals↗

PubMed1972

Ultrastructural characteristics of the "hairy cells" of leukemic reticuloendotheliosis.

The pathognomonic neoplastic reticulum cells, or "hairy cells" of leukemic reticuloendotheliosis from 6 patients were studied with the electron microscope. These cells demonstrated characteristic ultrastructural features which were distinctly different from those of lymphocytes, monocytes, or histiocytes. In 3 patients a distinctive ribosome-lamella complex was found. The biologic significance of this unusual cytoplasmic inclusion is still unknown. Its frequent presence in leukemic reticuloendotheliosis and its rarity in other neoplastic diseases suggest a substantial yet unexplained relationship between this complex and leukemic reticuloendotheliosis.

Bone Marrow Cells↗

PubMed2002

Reticuloendotheliosis in Hungarian partridge.

A large commercial flock of Hungarian partridge (Perdix perdix) experienced elevated mortality associated with a wasting disease in May 1998. Postmortem examination of females consistently revealed a distended crop and abnormal gray-white tissue infiltrating the wall of the crop and thoracic esophagus. Neoplasia in male partridge was observed in the liver. Microscopic examination of the crop and thoracic esophagus revealed transmural masses of immature lymphocytes with frequent mitotic figures. Similar cells were observed in the liver of affected males. Virus particles consistent in size and morphology with reticuloendotheliosis virions were observed in neoplastic lymphoid cells via electron microscopy. Reticuloendotheliosis virus was isolated from each of four blood samples. This disease has not previously been reported in Hungarian partridges. Hungarian partridge may represent a potential reservoir of infection for other gamebirds, including prairie chickens.

Animals↗

PubMed1978

Sites of integration of infectious DNA of avian reticuloendotheliosis viruses in different avian cellular DNAs.

The pattern of integration for the infectious DNA of two avian reticuloendotheliosis viruses whose DNA is not inactivated by digestion with the restriction endonuclease, Eco RI was determined. High molecular weight DNA from infected chicken, turkey and pheasant cells was digested with Eco RI, electrophoresed through agarose gels and assayed for infectivity. The same patterns of integration of infectious viral DNA were found for these species of avian cells infected at high or low multiplicities with two reticuloendotheliosis viruses. There were multiple sites of integration in acutely infected cells with concomitant cell death. There was a single site of integration in chronically infected cells with no cell death. There were more integrated infectious viral DNA molecules per cell in acutely infected cells than in chronically infected cells. These results are consistent with the hypotheses that the cell death in the acute phase of infection is a result of the integration of the infectious viral DNA at multiple sites, and that only those cells survive that have the infectious viral DNA integrated exclusively at the single site.

Cell Line↗

PubMed1981

Avian reticuloendotheliosis virus: identification of the hematopoietic target cell for transformation.

Non-virus-producing hematopoietic cells transformed in vitro by reticuloendotheliosis virus (REV-T) induce lethal "reticuloendotheliosis" when inoculated into histocompatible chickens. This is the first direct demonstration that an in vivo target cell of an avian acute leukemia virus can be transformed in vitro. The tumorigenic, REV-T-transformed non-virus-producing cells fail to express helper-virus-coded proteins. REV-T transformed tumorigenic cells therefore do not require helper-virus functions. Cells transformed in vivo or in vitro by REV-T have lymphoblastoid morphology and express low levels of terminal-deoxynucleotidyl-transferase activity and bursal-cell determinants. One clone synthesized Ig mu. The preferred target cells for REV-T transformation are therefore immature lymphoid cells that express B-cell determinants. We propose that the unique transforming sequence of REV-T be designated rel (lymphoid).

Animals↗

PubMed1982

Substitution of 5' helper virus sequences into non-rel portion of reticuloendotheliosis virus strain T suppresses transformation of chicken spleen cells.

The genome of the highly oncogenic avian retrovirus reticuloendotheliosis virus strain T (REV-T) differs from that of the helper virus reticuloendotheliosis virus strain A by a substitution (rel and a large deletion. Further deletions, constructed in vitro, within the helper-virus-related sequences of REV-T have little effect on the ability of the virus to transform chicken spleen cells in vitro. However, deletions that extend into rel abolish transformation. Substitution of helper-virus-related sequences for the deleted region in the non-rel portion of REV-T also abolishes transformation. Viruses with revertant phenotype were obtained both spontaneously and by construction in vitro from these substituted recombinants. The revertant viruses have various mutations, including deletions and insertions, in the helper-virus-related sequences. Thus the additional helper-virus-related sequences suppress expression of transformation in cis, and the deletion in REV-T seems necessary for expression of the transforming properties of the virus.

Animals↗

PubMed2006

Phylogenetic analyses indicate little variation among reticuloendotheliosis viruses infecting avian species, including the endangered Attwater's prairie chicken.

Reticuloendotheliosis virus infection, which typically causes systemic lymphomas and high mortality in the endangered Attwater's prairie chicken, has been described as a major obstacle in repopulation efforts of captive breeding facilities in Texas. Although antigenic relationships among reticuloendotheliosis virus (REV) strains have been previously determined, phylogenetic relationships have not been reported. The pol and env of REV proviral DNA from prairie chickens (PC-R92 and PC-2404), from poxvirus lesions in domestic chickens, the prototype poultry derived REV-A and chick syncytial virus (CSV), and duck derived spleen necrosis virus (SNV) were PCR amplified and sequenced. The 5032bp, that included the pol and most of env genes, of the PC-R92 and REV-A were 98% identical, and nucleotide sequence identities of smaller regions within the pol and env from REV strains examined ranged from 95 to 99% and 93 to 99%, respectively. The putative amino acid sequences were 97-99% identical in the polymerase and 90-98% in the envelope. Phylogenetic analyses of the nucleotide and amino acid sequences indicated the closest relationship among the recent fowl pox-associated chicken isolates, the prairie chicken isolates and the prototype CSV while only the SNV appeared to be distinctly divergent. While the origin of the naturally occurring viruses is not known, the avian poxvirus may be a critical component of transmission of these ubiquitous oncogenic viruses.

Amino Acid Sequence↗

PubMed1975

Isolation and characterization of viruses from natural outbreaks of reticuloendotheliosis in turkeys.

We have described the in vitro isolation of type-C RNA viruses from two outbreaks of a fatal neoplastic disease in turkeys we diagnosed as reticuloendotheliosis. The virus had a density of 1.16 g/ml in sucrose gradients, had a DNA polymerase capable of using both endogenous and exogenous (synthetic) templates, and was infectious in vitro for turkey and chick cells. The culture-propagated virus was oncogenic for turkeys. The virus isolates were unrelated to avian leukosis virus and antigenically identical to reticuloendotheliosis virus (REV) strain T. Thus our studies suggested that REV is a causative agent of naturally occurring, fatal leukosis in turkeys.

Animals↗

PubMed1980

Assembly of avian reticuloendotheliosis virus: association of the core precursor polypeptide with the intracellular ribonucleoprotein complex.

A virus-specific ribonucleoprotein complex is present in the cytoplasm of reticuloendotheliosis virus-transformed chicken bone marrow cells. This ribonucleoprotein complex contains viral reverse transcriptase activity and may represent a precursor to the budding virion. The major viral polypeptide associated with the ribonucleoprotein complex was a polypeptide with a molecular weight of 63,000. This protein exhibited a precursor-product relationship with the major reticuloendotheliosis virus structural core protein p29. Core polypeptides were not associated with the intracellular ribonucleoprotein complex. Thus, p29 was incorporated into the virion in the form of its precursor Pr63. The cleavage of Pr63 in the ribonucleoprotein complex was accomplished either during the budding process of shortly after the release of particles from the cell.

Animals↗

PubMed1980

Avian reticuloendotheliosis virus: characterization of the high-molecular-weight viral RNA in transforming and helper virus populations.

Reticuloendotheliosis virus strain T (REV-T) is a type C retrovirus known to transform avian fibroblasts, spleen cells, and bone marrow cells and to produce virulent reticuloendotheliosis in young chicks. Analysis of REV-T high-molecular-weight RNA by electrophoresis in denaturing gels and by electron microscopy revealed the presence of at least two classes of molecules. One class appeared in CH3HgOH gels to have a monomer length of 9.3 kilobases (kb); in electron microscopic spreads under mildly denaturing conditions, it existed as a typical retrovirus dimer, having a monomer length of 8.8 +/- 0.7 kb. The second class also existed as a dimer, with a monomer length of 5.7 kb in CH3HgOH gels. Hybridization with REVA-A 32P-labeled complementary DNA revealed a third size class of molecules (4.7 kb), which were not resolvable from the 5.7-kb class in electron microscope spreads and which comigrated with chicken 28S rRNA in denaturing gels. Only the 9.3-kb class was found in the reportedly nontransforming virus produced after infection of canine thymus cell line with REV-T. Thus, REV-T appears to be similar to the murine and feline sarcoma viruses and the avian acute leukemia viruses in that it consists of a nontransforming helper virus genome and a defective genome responsible for oncogenicity. Our previous results demonstrated the presence in REV-T and in uninfected chicken cellular DNA of some nucleotide sequences not found in virus produced by the canine line (S. Simek and N. Rice, J. Virol. 33:320--329, 1980). In this report we show by hybridization with highly specific 32P-labeled complementary DNAs that REV-T-specific sequences exist within the 5.7-kb genome. Since 32P-labeled complementary DNA synthesized from the canine-derived virus genome hybridized with all three classes of RNAs, we conclude that the 5.7-kb genome is a recombinant between some sequences found in the putative helper and some sequences specific to REV-T. As with the other oncogenic viruses mentioned above, these specific sequences appear to be derived from host DNA.

Base Sequence↗

PubMed1982

Genome of reticuloendotheliosis virus: characterization by use of cloned proviral DNA.

Reticuloendotheliosis virus is an avian type C retrovirus that is capable of transforming fibroblasts and hematopoietic cells both in vivo and in vitro. This virus is highly related to the three other members of the reticuloendotheliosis virus group, including spleen necrosis virus, but it is apparently unrelated to the avian leukosis-sarcoma virus family. Previous studies have shown that it consists of a replication-competent helper virus (designated REV-A) and a defective component (designated REV) that is responsible for transformation. In this study we used restriction endonuclease mapping and heteroduplex analysis to characterize the proviral DNAs of REV-A and REV. Both producer and nonproducer transformed chicken spleen cells were used as sources of REV proviral DNA; this genome was mapped in detail, and fragments of it were cloned in lambdagtWES.lambdaB. The infected canine thymus line Cf2Th(REV-A) was used as a source of REV-A proviral DNA. The restriction maps and heteroduplexes of the REV and REV-A genomes showed that (proceeding from 5' to 3') (i) REV contains a large fraction of the REV-A gag gene (assuming a gene order of gag-pol-env and gene sizes similar to those of other type C viruses), for the two genomes are very similar over a distance of 2.1 kilobases beginning at their 5' termini; (ii) most or all of REV-A pol is deleted in REV; (iii) REV contains a 1.1 kilobase segment derived from the 3' end of REV-A pol or the 5' end of env or both; (iv) this env region in REV is followed by a 1.9-kilobase segment which is unrelated to REV-A; and (v) the helper-unrelated segment of REV extends essentially all of the way to the beginning of the 3' long terminal repeat. Therefore, like avian myeloblastosis virus but unlike the other avian acute leukemia viruses and most mammalian and avian sarcoma viruses, REV appears to be an env gene recombinant. We also found that the REV-specific segment is derived from avian DNA, for a cloned REV fragment was able to hybridize with the DNA from an uninfected chicken. Therefore, like the other acute transforming viruses, REV appears to be the product of recombination between a replication-competent virus and host DNA. Two other defective genomes in virus-producing chicken cells were also cloned and characterized. One was very similar to REV in its presumptive gag and env segments, but instead of a host-derived insertion it contained additional env sequences. The second was similar (but not identical) to the first in its gag and env regions and appeared to contain an additional 1-kilobase inversion of REV-A sequences.

Animals↗

PubMed1988

Novel glycosylation pathways of retroviral envelope proteins identified with avian reticuloendotheliosis virus.

Previously, we identified two mature glycoproteins, gp90, the surface glycoprotein, and gp20, the transmembrane protein, from avian reticuloendotheliosis virus and an avian reticuloendotheliosis virus env gene-encoded intracellular polyprotein gPr77env, but the precise relationship of gPr77env to the mature envelope proteins was not determined (W.-P. Tsai, T.D. Copeland, and S. Oroszlan, Virology 155:567-583, 1986). In the present study, using metabolic labeling of viral proteins with [35S]cysteine, radioimmunoprecipitation, and carbohydrate structure analysis, we have identified a higher-molecular-weight endo-H-resistant env gene-encoded polyprotein designated gPr115env in addition to the endo-H-sensitive gPr77env. It appears that gPr77env is the primary polyprotein precursor, modified with mannosyloligosaccharides that are processed into sialic-acid-rich extraordinarily large complex-type carbohydrates (up to 17 kilodaltons for each N-linked site) on the gp90 domain but not on the gPr22 domain. In this process, gPr77env is converted into the apparently endo-H-resistant secondary polyprotein, gPr115env, which is rapidly processed into gp90 and gPr22. The proteolytic processing which occurs only after the appearance of an endo-H resistant precursor is now clearly demonstrated for a retrovirus. Some important aspects of carbohydrate structure, including the site-specific glycosylation, as well as the intracellular location and nature of the potential enzyme involved in the proteolytic cleavage of gPr115env are discussed.

Animals↗

PubMed1989

Replication-defective vectors of reticuloendotheliosis virus transduce exogenous genes into somatic stem cells of the unincubated chicken embryo.

Replication-defective vectors derived from reticuloendotheliosis virus were used to transduce exogenous genes into early somatic stem cells of the chicken embryo. One of these vectors transduced and expressed the chicken growth hormone coding sequence. The helper cell line, C3, was used to generate stocks of vector containing about 10(4) transducing units per ml. Injection of 5- to 20-microliters volumes of vector directly beneath the blastoderm of unincubated chicken embryos led to infection of somatic stem cells. Infected embryos and adults contained unrearranged integrated proviral DNAs. Embryos expressed the transduced chicken growth hormone gene and contained high levels of serum growth hormone. Blood, brain, muscle, testis, and semen contained from individuals injected as embryos contained vector DNA. Replication-defective vectors of the reticuloendotheliosis virus transduced exogenous genes into chicken embryonic stem cells in vivo.

Animals↗