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Two commercial flocks of Chinese partridge experienced increased mortality associated with a wasting disease at 120-day old in June 2006. Postmortem examination of dead chickens consistently showed visceral tissues mainly proventriculus, liver and spleen were diffuse enlargement. Microscopic examination revealed masses of immature lymphocytes with frequent mitotic figures were seen in various tissues including proventriculus, liver, spleen, kidney, heart, lung, thymus and intestine. Reticuloendotheliosis virus (REV) was isolated from each of four blood samples. Viral antigens were observed in cultured CEF (SPF embryos came from the Ji-nan poultry institute) inoculated blood samples via on indirect immunofluorescent assay. Three hundred bp fragments of LTR of REV obtained from liver samples of six chickens by PCR. This disease has not previously been reported in Chinese partridge. Chinese partridge may represent a potential reservoir of infection for other Chinese local chickens.

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.

Infection with chicken anaemia virus (CAV), a circovirus, can result in immunosuppression and subsequent increased susceptibility to secondary infections. This is the first report of impairment of pathogen-specific cytotoxic T lymphocytes (CTL) after natural and experimental infection of chickens with CAV and Marek's disease virus (MDV) or reticuloendotheliosis virus (REV). MDV- and REV-specific CTL were generated at 7 days post infection by 9-30-day-old-chickens that were positive for maternal antibodies to CAV at 9-17 days of age. Replication of CAV could not be demonstrated in these chickens using quantitative real-time polymerase chain reaction (PCR) and reverse transcriptase (RT)-PCR assays. In contrast, REV-specific CTL failed to develop when chickens negative for maternal antibodies at 9-17 days of age were infected. Infection with CAV at 45 days of age after CAV maternal antibodies had waned also caused a decreased REV-specific CTL response. In these chickens increased levels of CAV DNA of up to 107 copy numbers per micro g DNA and increased relative transcript levels of CAV by up to a factor of 106 were detected by quantitative real-time PCR and RT-PCR. Interleukin (IL)-1beta and IL-2 mRNA levels were not significantly affected by CAV infection at 7 or 14 days p.i. Similar assays for interferon-gamma (IFN-gamma) transcripts demonstrated a 10-fold increase in IFN-gamma mRNA levels at 7 days post infection following REV or REV + CAV infection, while CAV alone caused a two- to fourfold increase. These results show a strong link between CAV antibody status, CAV replication, and the ability to generate REV-specific CTL. It is likely that the immunosuppressive effects of subclinical infection have previously been underestimated.

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.

To determine whether there is any abnormalities of the p53 gene in chicken lymphoblastoid tumor cell lines derived from Marek's disease (MD), lymphoid leukosis, reticuloendotheliosis, and field tumors, some portions of p53 cDNA corresponding to core and C-terminal domains (nucleotide positions 277-1104 in the p53 open reading frame (ORF)) were sequenced. Several mutations were identified in both cell lines and field tumors. However, none of these mutations is localized at the "hot spot", which has been reported as the site for transformation-activating mutations. Moreover, partial cDNA clones with a 122-bp deletion in the p53 ORF were identified in two cell lines, MSB1 and MTB1 derived from MD tumors. Southern blot analysis showed that no deletion occurred in the genome of p53 in MSB1, indicating that deletion occurred at the transcriptional level. This deletion could cause a frame shift of the encoding p53 protein, possibly resulting in the generation of a functionally different p53 protein. However, we confirmed that p53 mRNA without deletion is also present in each of these cell lines. These mutations of the p53 gene and deletion in the p53 transcript may be ones of molecular changes specific to the transformation induced by MD virus.

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.

Twelve turkeys from a flock of 2,500 had cutaneous lesions somewhat resembling fowl pox. Lymphoid-like tumors were evident in livers and spleens. Closer examination of cutaneous lesions, and histopathological examinations indicated skin lesions were also infiltrative and not unlike reticuloendotheliosis. Electron micrographs revealed the presence of C-type virus particles.

Groups of 25 chickens free of maternal antibody to reticuloendotheliosis virus (REV) were inoculated with either third or seventh passage REV at either one or seven days of age. Some of the birds inoculated at day 1 with REV were inoculated with Salmonella typhimurium either concurrently or six or 13 days later while some of those inoculated with REV at day 7 were inoculated concurrently with S typhimurium. At day old, infection with S typhimurium alone caused the death of 12 of 25 chicks whereas in the dual infection, using the third passage REV, 18 of 25 birds died. Similarly no seven or 14 day old chickens died when challenged with S typhimurium alone, but previous day-old infection with REV caused a respective mortality of eight of 25 and five of 25 birds. With the seventh passage REV a similar pattern was seen. At day old S typhimurium infection alone killed seven of 25 birds whereas combined with virus the mortality was 14 of 25 and while S typhimurium alone killed none of 25 chicks infected at seven days old, the mortality in birds also infected with REV was 14 of 25. Combined virus and bacterial infections did not increase the proportion of feathering defects in birds surviving S typhimurium infections. There was a significantly higher proportion of feathering defects in birds infected with third passage virus compared with seventh passage virus. Although a higher proportion of birds had antibody responses to REV in the seventh than in the third passage group, there was no discernible difference in the effect the different viruses had on chickens' susceptibility to S typhimurium.

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.

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.

Replication of reticuloendotheliosis viruses (REV) in cultures of chicken and duck fibroblasts leads to some cell death soon after infection. This cell killing was used to develop a plaque assay for Trager duck spleen necrosis virus (TDSNV) on duck embryo fibroblasts. A normal replicative cell cycle was required for normal virus production and the development of cytopathic effects in chicken cells exposed to TDSNV. The latent period was about two days. Stationary chicken embryo fibroblasts could be infected by REV; DNA synthesis was required, but protein synthesis was not.

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.

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 naturally occurring lymphoproliferative disease was observed in a domestic flock of Muscovy ducks. Gross lesions were observed only in one of three ducks necropsied (in the small intestine). Microscopic lesions consisted of mononuclear cell infiltrates composed primarily of reticuloendothelial cells, mature lymphocytes, and plasma cells in livers, spleens, small intestines, peripheral nerves, and brains. Antibodies to reticuloendotheliosis virus were detected in sera of four ducks, whereas all six ducks examined lacked antibodies ot Marek's disease virus.

Velocity sedimentation and isopycnic density gradient centrifugation indicate that reticuloendotheliosis virus has a different mass and buoyant density than members of the avian tumor virus group. The group-specific antigen of the avian tumor virus group was not detected in concentrated and purified reticuloendotheliosis virus preparations.