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Reticuloendotheliosis Virus (REV) is an RNA virus belonging to the family Retroviridae and the genus Gamma Retrovirus. It mainly infects the immune systems of poultry such as chickens and turkeys. The genome of this virus can be stably integrated into vectors such as avian pox virus, resulting in the recombinant virus strain exhibiting complex pathogenic characteristics. As of 2020, research data shows that the positive rate of antibodies in some chicken farms has reached 21% -30%, and the immune suppression syndrome it causes seriously threatens the development of the poultry industry. Virus diagnosis mainly relies on techniques such as PCR amplification and immunofluorescence, and currently there are no specific prevention and control measures available. Laboratory diagnosis and research into viral prevalence and host immune response rely on serological methods, where the Reticuloendotheliosis Virus (T) Tissue Culture Antigen, derived from infected cell cultures, serves as a crucial reagent in assays like agar gel immunodiffusion (AGID) and enzyme-linked immunosorbent assay (ELISA) for detecting group-specific antibodies.
Figure 1. Schematic representation of REV proteins. (Chacón, Ruy D,et al, 2025)
Reticuloendotheliosis virus (REV) is a retrovirus that infects a wide range of avian species, including both wild birds and poultry. It belongs to the Gammaretrovirus genus and is associated with various clinical syndromes, primarily chronic and acute neoplasias, immunosuppression, and subclinical or asymptomatic infections. REV viral particles are spherical or slightly pleomorphic, measuring approximately 100 nm in diameter, and are enclosed by a lipid envelope with associated surface glycoproteins. Its genome consists of linear, positive-sense RNA, which is converted into double-stranded DNA during the proviral state. The REV genome is 8.2 to 8.4 kb in length and contains the gag, pol, and env genes, flanked by identical long terminal repeat (LTR) sequences. As a retrovirus, REV integrates into the genome of host cells. Notably, REV can also integrate into the genomes of other DNA viruses, forming viral chimeras, primarily with poxviruses and herpesviruses. These chimeric integrations or co-infections can lead to exacerbated or atypical clinical conditions and may compromise vaccine efficacy.
The disease outcome depends on the viral strain and host factors. Replication-competent REV strains (e.g., REV-A) often cause a runting disease syndrome characterized by stunted growth, necrotic lesions, and immunosuppression due to lytic infection of lymphoid tissues. In contrast, the replication-defective REV-T strain causes acute lymphomatous disease. Here, the helper virus provides the necessary proteins for replication, while REV-T's v-rel oncogene is the direct driver of transformation. The v-Rel protein hijacks the host NF-κB signaling pathway—a central regulator of immune response, inflammation, and cell survival—by forming abnormal complexes that constitutively activate or repress target genes, resulting in the rapid and fatal proliferation of transformed lymphocytes.
| Diagnosis | Details |
| Virus Characteristics | The virus particles are spherical with a diameter of about 100nm, and the surface of the capsule is distributed with gp90 glycoprotein. The genome contains gag, pol, and env genes, and the defective strain requires REV-A helper virus to complete replication. Sensitive to ether and ultraviolet radiation, deactivated for 30 minutes under pH 3.0 conditions. |
| Pathogenic Mechanism | Targeting splenic reticuloendothelial cells and inducing activation of endoplasmic reticulum stress signaling pathway. Upregulation of pro apoptotic factor Caspase-3 expression triggered by unfolded protein response. Inhibition of host cell MHC-I molecule expression leads to loss of immune surveillance function. |
Transmission of REV occurs through various routes. Vertically, the virus can be transmitted via semen from birds with persistent viremia. Horizontally, it spreads through close contact with feces, body fluids, or contaminated litter. Additionally, hematophagous insects and arachnids can transmit REV after feeding on infected blood, and mechanical transmission by insects has also been documented. The dissemination of chimerized viruses, such as the fowlpox virus (FWPV), further complicates control efforts due to the wide range of free-living hosts. Cases of REV outbreaks linked to contaminated vaccines underscore the need for stringent vaccine quality control.
Most REV studies focus on poultry, particularly chickens. Reports on waterfowl poultry are scarce, but some have documented increased mortality accompanied by lymphomas in visceral organs, such as in Anser anser and Cairina moschata. Similarly, in wild waterfowl, REV has been associated with morbidity and mortality in Branta sandvicensis and Phoebastria immutabilis in Hawaii, USA. REV has been reported in numerous countries, infecting both poultry and free-living birds, either alone or in coinfection with other pathogens. However, in South America, REV has been scarcely studied. Apart from Brazil, only serological reports exist in other countries, showing positivity rates ranging from 33.3% in Peru to 95% in Argentina. In Brazil, REV has been documented in commercial birds, backyard birds, and free-living birds. However, only two complete genomes have been sequenced from commercial birds in the country.
REV is an oncogenic and immunosuppressive virus capable of infecting various species across different avian orders. REV is associated with various clinical manifestations in birds, including runting disease syndrome, abnormal feathering, paralysis, and increased mortality. When birds develop chronic lymphomas or acute reticulum cell neoplasms, they often show few obvious clinical signs due to the rapid progression of the disease, which typically leads to death REV is a known threat to avian health, the scientific community still faces many unanswered questions. Comprehensive research efforts are needed to elucidate its pathogenesis, improve diagnostic tools, and develop effective control measures. Only through sustained investigation can we hope to mitigate the impact of this virus on both domestic and wild bird populations.
Reference
| Target | Cat. No. | Product Name | Host | |
| REV | DAG-WT5793 | Reticuloendotheliosis Virus (T) Antigen Concentrate | SPF chicken embryos | Inquiry |
| DAGC567 | Reticuloendotheliosis Virus (T) Tissue Culture | N/A | Inquiry | |
| DAGC568 | Reticuloendotheliosis Virus (T) Tissue Culture Antigen | N/A | Inquiry |
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