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Morphological and immunological studies of four cases of leukaemic reticuloendotheliosis are reported. The findings indicate that leukaemic reticuloendotheliosis is a monoclonal B cell neoplasm in which the leukaemic cell expresses either Kappa or lambda light chain and delta heavy chain determinants. The similarity between this disease and chronic lymphocytic leukaemia is discussed.
Cytotoxic chemotherapy often induces sustained, severe granulocytopenia in patients with leukemic reticuloendotheliosis. Many of the patients so treated subsequently develop serious infections. Poor marrow reserve has been implicated but lacks supporting evidence as the cause of the granulocytopenia. In six patients we studied with leukemic reticuloendotheliosis, bone marrow showed severe granulocytopenia, blood neutrophil response after intravenous hydrocortisone injection was poor, and leukocyte migration to the site of inflammation showed suboptimal neutrophilia and poor or no mononuclear response. Splenic hypersequestration and pooling were probably not important factors in causing neutropenia, since similar results were seen in patients without spleens. These findings suggest that in this disease the marrow granulocyte reserve and leukocyte mobilization are impaired and the neutropenia is due to poor granulocyte production and not to increased migration of leukocytes to tissues. Cytotoxic chemotherapy should be used with caution in patients with this disease.
A case of reticuloendotheliosis in a 7-year-old Gordon Setter is reported. Progressive weakness, debility, and diarrhea with melena were the presenting complaints. Clinical evaluation revealed splenomegaly, severe nonregenerative anemia, thrombocytopenia and leukopenia with many large blast cells in the peripheral blood. Necropsy revealed extensive involvement of bone marrow, spleen, liver, lymph nodes, kidneys, and adrenals. Gastric and duodenal ulcers were also present. The course, clinical findings and cellular characteristics of the case presented, closely resemble those reported in the syndrome of reticuloendotheliosis in cats.
Reticuloendotheliosis virus strain T (Rev-T) is a highly oncogenic retrovirus that induces a lethal lymphoma in young galliform birds and also transforms and immortalizes avian lymphoid cells in vitro. Rev-T presumably arose when a reticuloendotheliosis virus (Rev) incorporated a portion of the turkey c-rel gene into its genome, forming the v-rel oncogene. The predicted v-rel protein (p59v-rel) has 14 amino acid substitutions and 3 amino acid deletions relative to the predicted turkey c-rel protein. The 5' Rev env-derived amino-terminus of p59v-rel also has amino acid substitutions in codons 3, 6, and 9 relative to wild-type Rev-A env. To distinguish the critical alterations from the neutral ones, we made a mutation that resulted in a substitution of the 5' Rev env-derived amino-terminus by a single methionine, as well as several back-mutations, in the context of an otherwise wild-type v-rel and tested the transforming, immortalizing, and tumorigenic properties of the resulting proteins. All proteins tested retained the transforming, immortalizing, and tumorigenic functions of v-rel. Absence of the 5' Rev env-derived amino-terminus, as well as back-mutations of six of the amino acid changes present in the rel-derived amino-terminal and central regions of v-rel, reduced transformation efficiency. The mutations present in codons 3, 6, and 9 of p59v-rel showed complicated interactions in their activating effects on transformation efficiency. We also showed that loss of the immortalizing function did not abolish tumorigenesis by v-rel. We further showed that the primary transduction event involving the turkey c-rel gene could have occurred with a replication-competent Rev having v-rel-specific mutations in codons 3, 6, and 9 of the env gene.
The pathognomonic "hairy cell" of leukemic reticuloendotheliosis was studied for ultrastructural localization of tartrate-resistant acid phosphatase activity. The enzyme activity could not be demonstrated by Gomori's method, but it was readily demonstrated in the cytoplasmic vesicles and Golgi saccules of the hairy cell by substitution of naphthol AS-BI phosphoric acid for Na-beta-glycerophosphate of Gomori's medium. This apparent substrate specificity may be used as a marker for electron microscopic identification of the hairy cell, and may facilitate the study of histogenesis of leukemic reticuloendotheliosis.
Studies with transmission and scanning electron microscopes (TEM and SEM) were performed on specimens from patients suspected of leukemic reticuloendotheliosis (LRE), irrespective of the final diagnoses. The blood samples were fixed immediately in order to avoid in vitro changes of leukocytes. Leukemic reticuloendotheliosis cells demonstrated numerous long microvilli and pseudopods, whereas the immediately fixed lymphocytes demonstrated fewer, shorter microvilli and no pseudopods. These surface features distinguishing LRE cells from lymphocytes and monocytes were appreciated by both SEM and TEM. In addition, TEM revealed significant differences in the incidence of certain ultrastructural alterations. Whereas nuclear pockets were rare in lre cells, they were relatively frequent in lymphocytes of other hematologic disorders. The inclusions of ribosome-lamella complexes were not only more prevalent in patients with LRE but were seen in a higher percentage of leukemic cells from patients with LRE than in those from patients with other hematologic disorders. Electron microscopy can play a role in the laboratory diagnosis of LRE.
Reticuloendotheliosis virus strain A (REV-A) and chicken syncytial virus (CSV), two replication competent avian retroviruses, differ in the extent to which they induce a runting syndrome that includes anemia, lymphoid organ atrophy, and reduced body size. We have isolated an infectious clone of CSV, the less pathogenic of the two viruses, and compared it to REV-A. Partial DNA sequence analysis suggests that it differs from REV-A by no more than 1 to 2% at the nucleotide level. Analysis of viral interference indicates that these two viruses use the same cell receptor for infection of both fibroblasts and hematopoietic cells, DNA sequence of the CSV and REV-A long terminal repeats (LTRs) reveals that these structures differ principally by two small insertions (5 and 19 bp) present in the U3 region of REV-A. The larger of these may encode enhancer sequences that have been reported to influence transcription rates in vitro. Measurement of steady-state levels of viral RNA in infected cells, however, as well as circulating virus in infected chicks indicates that the different pathogenic responses elicited by these two viruses are not due to large differences in viral transcription or replication. Chimeric viruses were constructed in which the LTRs from one virus were used to express the structural genes of the second virus. Infection of 1-day-old chicks by parental virus as well as the reciprocal chimeric constructs demonstrated that the ability to induce both runting and bursal atrophy segregated with the structural genes of REV-A. Infection of birds with additional chimeric viruses in which the env genes of REV-A and CSV were exchanged indicated that the pathogenic response resulting from REV-A infection was due to at least two regions of the viral genome encoding structural genes.
Increased mortality and decreased egg production associated with disseminated lymphoma were observed in a turkey breeding flock for more than 20 weeks. A few unrelated meat turkey flocks, from the same integrator, experienced increased condemnation due to neoplasia in a few organs. Lymphoma was characterized by a uniform population of large lymphocytes with large vesicular nuclei containing one or two nucleoli and with little, faintly staining, basophilic cytoplasm. Neoplastic cells replaced normal tissue and were consistent with lesions seen with reticuloendotheliosis virus (REV) infection. Immunoperoxidase and fluorescent antibody staining characterized the neoplastic cells as CD3+, CD4+ and CD8- lymphocytes. Infection with REV was confirmed by virus isolation, polymerase chain reaction, serology and indirect fluorescent antibody. Poults hatched from these breeders tested positive for REV antibodies at hatch, but the performance of these flocks was normal and lymphoma was not observed. The origin of REV infection in this outbreak could not be determined. This is the first documented report of T-cell lymphomas associated with REV in commercial flocks. Furthermore, this is the first time that lymphomas have been characterized as T helper cells (CD3+ CD4+ and CD8-) in an outbreak of REV in turkeys.
Reticuloendotheliosis virus (REV) is widespread in the world. No related data has been reported in Taiwan. To determine the REV infection status, antibody determination and virus isolation were performed on chickens in Taiwan. The results revealed that serological flock prevalence for the REV antibody reached 92.8% (39/42) amongst breeders (> 16 weeks old). Two different REV isolates were identified by reverse transcriptase-polymerase chain reaction, electron microscopic, immunofluorescent, and western blot assays after isolation. One of these viruses was isolated from a broiler breeder farm and the other was isolated from a Taiwan Country Chicken farm. Despite their different origins, the percent identity of the nucleotide sequences of the env gene of these two isolates was 99.7%. These two strains were similar to the FPV-UI-REV strain, featuring 99.7% and 99.8% percent identity. Indeed, REV infection would appear to be quite common amongst chickens.
Two-day-old chicks were inoculated with one or ten doses of Marek's disease (MD) vaccine originated from the herpesvirus of turkeys (HVT) and contaminated with a reticuloendotheliosis virus (REV). As a result, they presented such symptoms as abnormality in the vane of remiges, undergrowth, anemia, and leg paralysis. These symptoms were the same as those induced by the same vaccine among chicks in the field. Control chicks which had been placed in the same house as those inoculated with the vaccine exhibited no abnormal signs. A persistent infection with REV was noticed in the vaccine-inoculated group. A horizontal infection with REV was the highest in the control group, which was followed by the group inoculated with one dose and that inoculated with ten doses in the order listed. The antibody response of chicks to HVT and MD virus was also inhibited by REV.
Over a period from spring to fall in 1974, a disease with delayed growth, anemia, abnormal feathers, and leg paralysis as main symptoms broke out in flocks of chickens inoculated with Marek's disease vaccine. A virus was isolated from affected birds in the field and the same lot of Marek's disease vaccine as inoculated into these birds. It had a common antigenicity to the T strain of reticuloendotheliosis virus (REV) and could not be discriminated from this strain on the basis of morphology or property. When chicks were inoculated with it, they presented essentially the same symptoms as the birds affected in the field. Since the disease was reproduced in this manner, it was presumed to have been caused by REV contained in the vaccine as contaminant. The virus persisted in the body for long time and also induced horizontal infection.
Abnormal feathers, characterized by thinness and increased transparency of the calamus and rachis, and loss of barbs, were induced at a high frequency by inoculating day-old chicks with reticuloendotheliosis virus (REV) propagated in chicken-embryo fibroblast (CEF) cultures. The few birds that survived inoculation with oncogenic stock of REV derived from liver tissue of an infected chick developed similar abnormalities. Lesions of an inflammatory-degenerative type were observed in close association with the presence of viral antigen and numerous c-type virus particles, characteristic of REV, in the intermediate and cylindrical cell layers of all abnormal feathers examined. These findings, first detected in the intermediate and cylindrical cell layers of developing feathers 6--9 days after infection, suggest that degeneration and necrosis of feather-forming cells result from productive infection of REV, resulting in the development of the abnormal feathers.
A specific micro-complement-fixation procedure for assay of avian reticuloendotheliosis viruses (REV), designated by use as the COFAR test, was compared with an assay based on immunofluorescent (IF) antibody staining of infected chick embryo fibroblasts. Endpoint titrations in which REV strain T, chick syncytial virus, and spleen necrosis virus were used indicated that cultures infected with limiting dilutions of each strain were positive by both procedures within 6 days. Depending on cell density, infection of 2 to 9% of the cells cultured produced an unambiguous positive response (titer greater than or equal to 1:2) with COFAR test. When both tests were used in a study on the transmission and in vivo status of ducks infected with spleen necrosis virus, COFAR was no less, possibly more, sensitive than IF for detecting infection in cultures inoculated with plasma.
Reticuloendotheliosis virus (REV) was isolated at 21 weeks from a flock of breeder turkeys with lymphoid neoplasms. Except for about 2% mortality due to tumors mainly between 20 and 30 weeks of age, the livability and egg production of the flock were normal. Egg transmission as a source of infection seemed unlikely, because no REV antibodies or production problems were observed in two sister flocks (hatchmates) and in three progeny flocks, and because eggs obtained from the breeder flock at 45 weeks lacked REV group-specific antigen and produced poults negative for REV infection. The virus isolate, designated REV strain 339, produced an acute neoplastic disease when inoculated into young chickens.
Cytotoxic T lymphocytes were functionally demonstrated in spleen cells from chickens 7 days post inoculation with reticuloendotheliosis virus using a Cr-release assay. Major histocompatibility complex (MHC)-restricted cytotoxicity was demonstrated using effector and target cells from two different strains of chickens of known avian MHC haplotype. Anti-viral specificity was shown and in vivo generation of MHC-restricted cytotoxicity was evaluated. Cytotoxic T cells were distinguished from macrophages and natural killer cells. Their cytotoxicity was not antibody dependent. Higher levels of cytolysis were found with cytotoxic T cells from embryonally bursectomized vs. intact chickens over a large range of effector to target cell ratios. Using monoclonal antibodies, cytotoxic T cells were further defined as Ia+ T cells by immunofluorescence, antibody plus complement-mediated lysis of effector cells and blocking of cytolysis in the Cr-release assay.
Chickens inoculated as embyros or at hatching with the chick syncytial strain of reticuloendotheliosis virus developed a high incidence of lymphoid neoplasms between the 17th and 43rd weeks of age, involving principally the liver and bursa of Fabricius. On the basis of organ distribution, latent period, pathology and surface IgM production, the lymphomas closely resembled those of lymphoid leukosis. One inoculated chicken developed a myxosarcoma. No tumors were observed in uninoculated controls. The tumor-bearing chickens were free of infection with Marek's disease virus and exogenous avian leukosis virus (ALV) of subgroups A, B, C or D. However, the chickens were known to express endogenous ALV genes to varying degrees.
Chickens of lines 6(3) and 151(5) X 7(1) were inoculated with the chick syncytial strain of reticuloendotheliosis virus (REV) or with the Rous-associated virus-I of avian leukosis virus (ALV) at hatching. At 4, 10, 16, and 36 weeks post inoculation (PI), chickens were tested for REV- and ALV-induced viremia and antibody. The incidence of REV- or ALV-induced bursa-associated lymphomas in line 6(3) chickens was compared with that in line 151(5) X 7(1) chickens. Inoculation of REV at hatching resulted in immunological tolerance to the virus in line 6(3) but not in line 151(5) X 7(1) chickens. Between 70% and 100% of line 6(3) chickens remained viremic and lacked REV antibody throughout the experimental period of 36 weeks. In contrast, ALV-inoculated chickens of both lines had antibody by 16 weeks PI. The frequencies of REV- and ALV-induced bursa-associated lymphomas in line 6(3) chickens were significantly lower than in line 151(5) X 7(1) chickens. Further, the incidence of bursa-associated lymphomas induced by REV in line 151(5) X 7(1) chickens was significantly lower than that induced by ALV. These results suggest that: (1) the genetic constitution of the host may influence the immunological response to REV infection; (2) chickens resistant to ALV-induced bursa-associated lymphomas are equally resistant to such lymphomas induced by another unrelated avian retrovirus, REV; and (3) ALV is a more potent inducer of bursa-associated lymphomas than REV.
Reticuloendotheliosis virus strain T (REV-T)-transformed cells gave rise spontaneously to variants which secrete a factor that forms a distinct visible ring of precipitation (halo) surrounding colonies grown in soft agar. An Mr 15,000 protein was produced at higher levels by halo variants than by nonhalo-producing cells. An assay designed to detect the formation of precipitates enabled purification of an Mr 15,000 protein, p15, from serum-free medium conditioned by the growth of REV-T-transformed hematopoietic cells. Fractions enriched in p15 permitted the growth of REV-T-transformed cells under conditions where they normally failed to proliferate.