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PubMed1990

Reduced duck hepatitis B virus viraemia in ducklings coinfected with the immunodepressive reticuloendotheliosis virus.

Coinfection of avian hosts by duck hepatitis B virus (DHBV) and reticuloendotheliosis virus (REV) was studied to assess the effect of immunodepression by REV on the replication of DHBV. One-day-old ducklings, domestic chickens, and turkey poults were inoculated either with DHBV or DHBV and REV and were bled and weighed at regular intervals. DHBV infection as manifested by viraemia and DHBV DNA in liver was established only in ducklings. All chickens and turkeys were negative for DHBV DNA in serum and liver. However, ducklings coinfected with REV showed a delayed onset and reduced level of viraemia compared to ducklings infected only with DHBV. The narrow host range of DHBV was confirmed even in immunodepressed species. It is suggested that the reduction in DHBV viraemia in ducklings was due to factors not involving the specific immune system.

Animals↗

PubMed1997

Field and vaccine strains of fowlpox virus carry integrated sequences from the avian retrovirus, reticuloendotheliosis virus.

For baculoviruses and herpesviruses, integration of transposons or retroviruses into the virus genome has been documented. We report here that field and vaccine strains of fowlpox virus (FPV) carry integrated sequences from the avian retrovirus, reticuloendotheliosis virus (REV). Using PCR and hybridization analysis we observed that vaccine and field strains of FPV carry REV sequences integrated into a previously uncharacterized region of the right 1/3 of the FPV genome. Long-range PCR, hybridization, and nucleotide sequence determination demonstrated that one vaccine strain (FPV S) and recently isolated field strains carry a near-full-length REV provirus. For another vaccine strain (FPV M) a rearranged remnant of the LTR was found at the same insertion site. By Western blotting and reverse transcriptase assays we were unable to demonstrate free REV in supernatants of FPV S cultures. The near-full-length REV provirus integrated into the FPV genome is infectious since FPV S DNA gave rise to REV upon transfection into chicken embryo fibroblasts. Upon infection of chickens with FPV S, all chickens developed high-titered antibodies to REV, and REV was isolated from the blood of half of the inoculated chickens. Our observations add to the list of targets for retrovirus integration into DNA virus genomes. The integration of a near-full-length, and apparently infectious, REV provirus into FPV provides additional transmission routes for the retrovirus by way of the infectious cycle of FPV, including the possibility of mechanical transmission by biting insects since FPV is believed to be transmitted by this route. For large DNA viruses, including the poxviruses, retrovirus integration with attendant possibilities of gene transduction may be an important mechanism for virus evolution, including the acquisition of cellular genes with the potential to modify virus virulence and pathogenicity.

Animals↗

PubMed1987

Serologic differences among nondefective reticuloendotheliosis viruses.

Antigenic relationships among 26 isolates of reticuloendotheliosis virus (REV) obtained from several avian species were compared by cross neutralization tests with polyclonal chicken sera and by immunofluorescent assays with monoclonal antibodies to REV strain T. The isolates were all strongly related by neutralization assays and thus probably constitute a single serotype. However, 3 antigenic subtypes were suggested by minor but distinct differences in neutralization titers. The validity of these 3 subtype designations was confirmed by differential reactivity of viral isolates to selected monoclonal antibodies. Subtype-associated differences in serum antibody titers were noted following the inoculation of chickens with the REV isolates.

Animals↗

PubMed1987

Sequence instability in the long terminal repeats of avian spleen necrosis virus and reticuloendotheliosis virus.

Sequence divergence between the 3' long terminal repeats (LTR) of avian reticuloendotheliosis virus (REV), deletion variant proviral clone 2-20-4, and spleen necrosis virus (SNV)-proviral clones 14-44, 60, and 70-was found to involve two classes of base substitutions: low-frequency interspersed and high-frequency clustered substitutions. Clones 2-20-4 and 14-44 have diverged 4.4% owing to low-frequency substitutions. In contrast, two high-frequency substitution segments have diverged by 30% and 29%, respectively. Clustered substitutions appear to be located either within or next to tandem repeats, suggesting their introduction concomitant with sequence deletions and duplications commonly associated with such repeats. A new 19-bp tandem repeat is found in clone 2-20-4. Its sequence could have evolved from the 26-bp repeats found in the SNV clones.

Base Composition↗

PubMed2006

Sequence analysis for the complete proviral genome of reticuloendotheliosis virus Chinese strain HA9901.

The genomic DNA extracted from chicken embryo fibroblast (CEF) infected with a Chinese field isolate HA9901 of reticuloendotheliosis virus (REV) was used as the template to amplify the REV proviral genomic cDNA by PCR with 6 pairs of primers according to published sequences. Six overlapping fragments were amplified, cloned into the TA vector and sequenced, including a fragment which was amplified from the circular proviral cDNA and covering both 5'- and 3'-ends. The complete sequence of the whole genome was established and analyzed with a DNAstar software. Comparisons of the sequence with two other strains demonstrated that the genomes of REV were relatively conservative, the homogenecity for all genes or LTR fragments of the 3 strains was over 92%, no matter whether they were isolated from different species and regions in different years. But, the homology of Chinese strain HA9901 to a fowl pox virus-associated strain from Chickens was higher than that to strain SNV isolated from ducks.

Animals↗

PubMed1985

Purification and chemical and immunological characterization of avian reticuloendotheliosis virus gag-gene-encoded structural proteins.

Five gag-gene-encoded structural proteins, designated p12, pp18, pp20, p30, and p10 were purified from replication-competent avian reticuloendotheliosis-associated virus (REV-A) by high-performance liquid chromatography complemented with chloroform-methanol extraction and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Based on amino acid composition and NH2- and COOH-terminal sequence analysis p12, pp18, p30, and p10 are distinct from one another, whereas pp20 is likely identical to pp18 in primary structure. The p12 was resistant to Edman degradation and was found to be myristylated at the NH2-terminal amino group. Sequence comparisons among the retrovirus family show that pp18/pp20 and p10 are, respectively, homologs of phospho-proteins and nucleic acid-binding proteins. A comparison of terminal sequences with the nucleotide sequence of spleen necrosis virus (SNV) revealed that the gag genes of SNV and REV-A are highly conserved; together with the identification of REV-A gag-precursor polyprotein, Pr60gag in immunoprecipitates of radiolabeled cell lysates, this comparison also led to the establishment of the organization of Pr60gag, viz., NH2-p12-pp18-p30-p10-OH. Sequence comparisons show that REV-A/SNV is related to mammalian type C viruses: the pp18-p30 region is most homologous to the macaque/colobus group and least to simian sarcoma virus (SSV), whereas both the 5'- and 3'-gag regions (i.e., p12 and p10) are clostest to SSV. Immunological studies using monospecific antisera and Western-blot analysis showed that antigenic determinants of REV-A p30 are conserved in most of mammalian type C and type D viruses, but those of REV-A p12 are shared only with simian sarcoma-associated virus (SSAV) and endogenous viruses of macaques.

Amino Acid Sequence↗

PubMed1986

Biosynthesis and chemical and immunological characterization of avian reticuloendotheliosis virus env gene-encoded proteins.

Two glycosylated proteins designated gp90 and gp20 were purified from replication-competent avian reticuloendotheliosis associated virus (REV-A). The N-terminal sequences of gp90 and gp20 were determined and found to match the REV-A-env-gene sequence. The alignments of the determined amino acid sequences with the predicted sequence indicate that gp20 and gp90 are the REV-A-encoded viral transmembrane and surface glycoprotein, respectively, and predict a signal peptide of 36 residues on the 5' end of the env-gene. Furthermore, gp90 of REV-A was detected by Western blot analysis with antibodies to a tridecapeptide corresponding to an env-gene nucleotide segment immediately preceding gp20 and thus representing the C-terminal portion of gp90. The env-gene precursor polyprotein gPr75-79env and Pr22(E), the precursor to gp20 and p2(E) were identified in the infected cells by monospecific antibodies raised against purified gp20. Thus the organization of gPR75-79env is likely to be N-gp90-gp20-p2(E), resembling that of M-MuLV gp85env. Sequence comparisons showed that the env gene of REV-A is highly related to both baboon endogenous virus and Type D retroviruses. In Western blot analyses, antibodies to REV-A gp20 cross-reacted with a panel of mammalian Type C and Type D viruses. Evolutionary aspects of these findings are discussed.

Amino Acid Sequence↗

PubMed1987

The transforming protein of avian reticuloendotheliosis virus is a soluble cytoplasmic protein which is associated with a protein kinase activity.

We have identified the product (p57v-rel) of the transforming gene, v-rel, of avian reticuloendotheliosis virus (REV-T) using antisera generated against nonoverlapping sequences representing the middle and carboxy-terminal regions of the v-rel protein expressed in Escherichia coli (N.K. Herzog and H.R. Bose, Jr., 1986, Proc. Natl. Acad. Sci. USA 83, 812-816). The amino-terminal region of the v-rel protein was also expressed in E. coli and used to generate antisera. The immunoglobulin-enriched fractions of these antisera were used to determine the subcellular location of p57v-rel in REV-T transformed lymphoid cells. Cells were fractionated into nuclear, mitochondrial, microsomal, and cytoplasmic fractions. The majority of p57v-rel was found in the cytoplasm. Examination of REV-T transformed lymphoid cells labeled with 32Pi revealed that the majority of the phosphorylated form of the v-rel protein was also found in the cytoplasm. Indirect immunofluorescence of REV-T transformed cells gave a diffuse cytoplasmic pattern indicating that p57v-rel was not associated with any discrete cellular organelle. The distribution of p57v-rel was similar in REV-T transformed lymphoid cells labeled with [35S]methionine for short and long periods of time, suggesting that p57v-rel is a soluble cytoplasmic protein throughout its lifetime. The v-rel protein was phosphorylated when immune complexes precipitated from transformed cells with the immunoglobulin fractions obtained from antisera against the amino-terminal, middle, and carboxy-terminal regions of v-rel were incubated with [gamma-32P]ATP and Mn2+. The phosphorylation of p57v-rel in the in vitro immune complex kinase assay was inhibited when the immunoglobulin-enriched fraction of these antisera was preincubated with the homologous v-rel fusion proteins. Preincubation with heterologous proteins did not block the phosphorylation of p57v-rel. These observations suggest that p57v-rel is associated with a protein kinase activity. Most of the kinase activity was found in the soluble cytoplasmic fraction of transformed cells. The transforming protein encoded by v-rel is a relatively stable protein with a half-life of approximately 7 to 8 hr in transformed lymphoid cells.

Cell Transformation, Viral↗

PubMed1988

Site-directed cytotoxic antibody against the C-terminal segment of the surface glycoprotein gp90 of avian reticuloendotheliosis virus.

The major mature env-gene products of avian reticuloendotheliosis-associated virus (REV-A) are the surface glycoprotein (gp90) and the transmembrane protein (gp20). We have previously reported that gp90 was detected in the REV-A virus by Western blot analysis as well as in the REV-A-infected cells by radioimmunoprecipitation with antibodies raised in rabbits against the gp90 C-terminal tridecapeptide which was predicted from the nucleotide sequence (Wilhemsen et al., J. Virol., 52, 172, 1984). We have now shown that this antibody detected antigens on the REV-A-infected cells by fluorescence-activated cell sorter (FACS) analysis, and conferred specific cytotoxic effects on the infected cells in the presence of rabbit complement using the chromium release assay. These results clearly indicate that the C-terminal epitope of gp90 is situated on the surface of the REV-A-infected cells and accessible to site-directed antibodies which cause cytotoxicity by activating the complement system. The possible in vivo roles of this antibody are discussed.

Animals↗

PubMed1989

Expression of avian reticuloendotheliosis virus envelope confers host resistance.

We constructed two reticuloendotheliosis virus (REV) envelope gene expression plasmids, one containing the REV-A envelope gene, the other the spleen necrosis virus (SNV) envelope gene. Cell lines were generated by transfecting each of the REV envelope plasmids into D17 cells, a canine cell line. The levels of REV envelope glycoprotein in the cell lines were assayed by immunoprecipitating the envelope glycoproteins from lysates of cells that were labeled with [35S]methionine. Virological challenge assays determined the degree of resistance of each of the cell lines to REV-A or SNV infection. The expression of either envelope gene protected the cells from infection by either REV-A or SNV virus. Several cell lines were significantly more resistant to REV infection than the parental D17 cells, and two lines were 25,000-fold more resistant, approaching the resistance of REV-infected D17 cells to reinfection. The resistant cell lines were not able to confer resistance to susceptible cells by cocultivation. The level of resistance was correlated with the uniformity of expression of the REV envelope glycoproteins by the individual cells in a cell line and not with the absolute level of expression by the population of cells.

Animals↗

PubMed1994

Syngeneic lysis of reticuloendotheliosis virus-transformed cell lines transfected with Marek's disease virus genes by virus-specific cytotoxic T cells.

Cell-mediated immune responses against Marek's disease virus (MDV) antigens were examined using reticuloendotheliosis virus (REV)-transformed cell lines of two haplotypes (B19B19 and B13B13). These cell lines were stably transfected with cloned fragments of MDV DNA resulting in the expression of the MDV-specific phosphoprotein pp38. Effector cells were obtained from P2a (B19B19) and S13 (B13B13) chickens at 7 days post inoculation with REV, oncogenic or attenuated serotype 1 MDV (JM-16/O and JM-16/A, respectively), serotype 2 MDV (SB-1), or herpesvirus of turkeys (HVT). Transfection of MDV genes did not influence the expression of Class I major histocompatibility complex antigens. The optimal effector to target cell ratio was determined to be 100:1. REV-sensitized effector cells lysed REV cell lines and REV cell lines transfected with MDV DNA in a syngeneic fashion. Effector cells from chickens inoculated with JM-16/O, JM-16/A, SB-1 or HVT lysed only the syngeneic, transfected cell lines, but not the parent REV cell lines. The percentage specific release caused by the MDV-sensitized effector cells was low, but statistically significant.

Animals↗

PubMed1993

Flow cytometric analysis of the neutralizing immune response against infectious bursal disease virus using reticuloendotheliosis virus-transformed lymphoblastoid cell lines.

Infectious bursal disease virus (IBDV) is a lymphotropic virus with cytocidal effect on B lymphocytes of the bursa of Fabricius. We investigated the susceptibility of clonal populations of reticuloendotheliosis virus-transformed chicken B lymphocytes of both spleen and bursal origin to IBDV infection. The infected cells were metabolically-labelled and the viral polypeptides were analyzed by immunoprecipitation using monoclonal antibodies (MAbs). Virus adsorption and the effects of neutralizing convalescent antisera and MAbs on virus attachment were studied using flow cytometry. The results of the study indicate firstly that the transformed B cells support virus replication and provide an efficient system for studying IBDV-lymphocyte interactions. Secondly, results obtained also showed that the most potent neutralizing antibodies may not be those involved in preventing the receptor-mediated viral attachment but rather those involved in the inhibition of downstream events such as virus penetration or uncoating.

Animals↗

PubMed1996

A non-radioactive method for identifying enzyme-amplified products of the reticuloendotheliosis proviral env and LTR genes using psoralen-biotin labelled probes.

A novel polymerase chain reaction (PCR) system based on the env gene of reticuloendotheliosis virus (REV) strain REV-A for the detection of proviral DNA is described. The designed PCR product of 807 bp was identified using an internal probe of 278 bp produced by nested PCR from REV-infected DNA CEF. The env-gene PCR was then compared with the previously described PCR for proviral REV-long terminal repeat and the PCR product served also as the probe. The probes were labelled with the psoralen-biotin system by photoactivation and the southern blot hybridization signal was detected colorimetricaly. The advantages of using a non-radioactive means of probe labelling were demonstrated clearly in that study, as well as the effective labeling of probes with psoralen-biotin and the simple colorimetric method of detection. The env-gene PCR detected all eleven REV strains used in the study. These included three REV prototype strains and eight Israeli REV isolates. Both PCR systems had similar levels of sensitivity.

Animals↗

PubMed1996

Detection of contamination of vaccines with the reticuloendotheliosis virus by reverse transcriptase polymerase chain reaction (RT-PCR).

The reverse transcriptase polymerase chain reaction (RT-PCR) was applied to detect contamination of Marek's disease (MD) vaccine with reticuloendotheliosis virus (REV). The env primers were used for the 1st RT-PCR to amplify the DNA fragments of REV-A and -T. The rel and env primers were used for nested-PCR to confirm the sites deleted from REV-T and REV-A. Specific amplification products were detected in the 1st RT-PCR with these primers. By nested PCR with the env and the rel primer pairs, the products originating from REV-A and -T were identified. This system, using the env primer pairs, showed a specific amplification with several REV strains (REV-T, DE, CE, KI and 0202), but no amplified product was detected with MDV, NDV, IBV or ILTV. The 1st RT-PCR detected the virus in a concentration of 10(3) in 50% fluorescent antibody infectious dose per ml (FAID50/ml) and the nested PCR detected 10(1) FAID50/ml virus. The sensitivity of the RT-PCR system was found to be higher than that of the FA assay. This system provides a rapid, sensitive and specific method for detection of contamination of MD vaccines with REV-RNA, and it may be applied for quality control of live vaccines.

Animals↗

PubMed1992

Reticuloendotheliosis virus long terminal repeat elements are efficient promoters in cells of various species and tissue origin, including human lymphoid cells.

Promiscuous transcriptional activity of the reticuloendotheliosis virus (REV) long terminal repeat (LTR) was detected in transient expression assays using LTR-chloramphenicol acetyltransferase-encoding gene chimeras, and cells of diverse species and tissue type; levels of expression from two different REV LTRs correlate with reports of pathogenicity of the respective viruses in vivo. REVs do not encode a transactivator targeted to the viral LTR, and cells infected with Marek's disease virus, a herpesvirus with an overlapping host range, do not express factors that preferentially enhance expression from REV or avian sarcoma/leukemia virus LTRs. REV LTRs work efficiently in human lymphoid cells, and are viable alternatives to promoters commonly used for expression of cloned genes. They may also prove useful in the identification of new, ubiquitous cellular transcription factors.

Animals↗

PubMed1984

Influence of reticuloendotheliosis on the severity of Eimeria tenella infection in broiler chickens.

Broiler chickens free of maternal immunity to reticuloendotheliosis virus (REV) were used in the experiment. Two groups of 25 chickens were inoculated with REV at one day of age. One of these groups and another group of 25 chickens were inoculated with Eimeria tenella sporulated oocysts at 7 days of age. Chickens inoculated with E. tenella showed bloody diarrhoea from 12 to 14 days of age. Six out of 25 chickens died (P less than 0.05) at 13 and 14 days of age in the dual infected group. At 14 days of age, when chickens were killed, the lesion score in the combined infection group, was statistically different from that in the chickens inoculated with E. tenella alone. Also the weights of the bursa of Fabricius and thymus were lower in the two REV infected groups than in the controls. Although REV infection alone adversely affected the weight gain and feed conversion, with combined infection this effect was much greater. Following REV inoculation most of the chickens showed feathering defects and all the examined chickens were viraemic at 21 days of age. At the same age, all but one chicken failed to show precipitating antigenaemia and about one-half of these chickens showed a very low serum neutralisation titre. None of these chickens showed precipitating antibodies.

Animals↗

PubMed1987

Clinical effects, virological and serological responses in chickens following in-ovo inoculation of reticuloendotheliosis virus.

Six-day-old embryonated specific pathogen free chicken eggs were inoculated with reticuloendotheliosis virus (REV) into the yolk sac and were incubated until they hatched. The hatchability of eggs inoculated with REV was significantly less (P less than 0.025) than that of media-inoculated controls. Although there were no significant differences in the body weights of these chickens at hatching, there were differences (P less than 0.001) at 6, 25 and 51 days of age between the infected and control chickens. Six of 10 chickens hatched from eggs inoculated with REV had feathering defects at 6 days of age. All chickens hatched from infected eggs had cell-free viraemia and antigenaemia, but not precipitating antibodies. Some of these chickens had very low neutralising antibody titres (less than 45) when examined at 25 and 37 days of age, as did all 10 chickens at 51 days of age. A low rate of horizontal transmission was indicated by the detection of antibodies at 37 and 51 days of age in chickens running in contact with the chickens hatched from eggs inoculated with REV.

Animals↗

PubMed2006

Full genome sequence and some biological properties of reticuloendotheliosis virus strain APC-566 isolated from endangered Attwater's prairie chickens.

Reticuloendotheliosis virus (REV) causes runting, high mortality, immunosuppression, and chronic neoplasia associated with T and/or B cell lymphomas in a variety of domestic and wild birds, including Attwater's prairie chickens (APC) (Tympanuchus cupido attwateri). The complete proviral sequence of a recent REV isolate from APC (REV APC-566) was determined. This virus was isolated from an APC maintained in captivity in a reproduction program intended to avoid its extinction. REV APC-566 was determined to be oncogenic in Japanese quail (Coturnix coturnix japonica), chickens (Gallus gallus) and turkeys (Meleagris gallopavo). Immune responses against bacteria and viruses were significantly reduced in turkeys infected with REV APC-566. The proviral genome is 8286 nucleotides in length and exhibits a genetic organization characteristic of replication-competent gammaretroviruses. The REV APC-566 provirus contains two identical long terminal repeats (LTR) and a complete set of genes including gag, gag-pol and env. As previously reported, alignments with other REV sequences showed high similarity with sequences found in the gag and pol genes from other REVs. The REV APC-566 env gene showed high nucleotide sequence homology with REV sequences inserted in fowl poxvirus (99.8%), and with spleen necrosis virus (SNV) (95.1%). Sequences coding for a previously reported immunosuppressive peptide contained in the transmembrane region of the env gene are well conserved among all REV sequences analyzed. The LTR was the most divergent region, exhibiting various deletions and insertions. REV APC-566 has a unique insertion of 23 bp in U3 and shares deletions of 19 and 5 bp with chicken syncytial virus and REV inserts in fowlpox virus.

Amino Acid Sequence↗