ArticleJournal of virology2012
A 205-nucleotide deletion in the 3' untranslated region of avian leukosis virus subgroup J, currently emergent in China, contributes to its pathogenicity.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- A novel recombinant ALV-K carrying ALV-J-derived LTR, pol, and 3'UTR from Chinese indigenous chicken breeds exhibits enhanced replication and increased hemangioma-associated pathogenicity.BMC veterinary research · 2026Article
- Isolation and identification of a highly oncogenic subgroup J avian leukosis virus strain from Chinese black chickens.Poultry science · 2026Article
- N6-methyladenosine modification of the subgroup J avian leukosis viral RNAs attenuates host innate immunity via MDA5 signaling.PLoS pathogens · 2025Article
- Isolation and molecular characterization of subgroup J avian leukosis virus in native chicken breeds of China during 2022-2025.Frontiers in microbiology · 2025Article
- N123I mutation in the ALV-J receptor-binding domain region enhances viral replication ability by increasing the binding affinity with chNHE1.PLoS pathogens · 2024Article
- 3'UTR of ALV-J can affect viral replication through promoting transcription and mRNA nuclear export.Journal of virology · 2023Article
- Molecular evolution, diversity, and adaptation of foot-and-mouth disease virus serotype O in Asia.Frontiers in microbiology · 2023Article
- Semen extracellular vesicles mediate vertical transmission of subgroup J avian leukosis virus.Virologica Sinica · 2022Article
- Chicken hepatomegaly and splenomegaly associated with novel subgroup J avian leukosis virus infection.BMC veterinary research · 2022Article
- Article
- Gp37 Regulates the Pathogenesis of Avian Leukosis Virus Subgroup J via Its C Terminus.Journal of virology · 2020Article
- Genetic Determinants of Altered Virulence of Type O Foot-and-Mouth Disease Virus.Journal of virology · 2020Article
- Isolation and Identification of Subgroup J Avian Leukosis Virus Inducing Multiple Systemic Tumors in Parental Meat-Type Chickens.Frontiers in veterinary science · 2020Article
- A novel recombinant avian leukosis virus isolated from gamecocks induced pathogenicity in Three-Yellow chickens: a potential infection source of avian leukosis virus to the commercial chickens.Poultry science · 2019Article
- Article
- The emerging novel avian leukosis virus with mutations in the pol gene shows competitive replication advantages both in vivo and in vitro.Emerging microbes & infections · 2018Article
- Residues 28 to 39 of the Extracellular Loop 1 of Chicken NaJournal of virology · 2018Article
- Full-length genome sequence analysis of four subgroup J avian leukosis virus strains isolated from chickens with clinical hemangioma.Virus genes · 2017Article
- Complete genome sequencing and characterization revealed a recombinant subgroup B isolate of avian leukosis virus with a subgroup J-like U3 region.Virus genes · 2017Article
- Avian leukosis virus subgroup J induces VEGF expression via NF-κB/PI3K-dependent IL-6 production.Oncotarget · 2016Article
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8 authors.
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Abstract
In the past 5 years, an atypical clinical outbreak of avian leukosis virus subgroup J (ALV-J), which contains a unique 205-nucleotide deletion in its 3' untranslated region (3'UTR), has become epidemic in chickens in China. To determine the role of the 205-nucleotide deletion in the pathogenicity of ALV-J, a pair of viruses were constructed and rescued. The first virus was an ALV-J Chinese isolate (designated HLJ09SH01) containing the 205-nucleotide deletion in its 3'UTR. The second virus was a chimeric clone in which the 3'UTR contains a 205-nucleotide sequence corresponding to a region of the ALV-J prototype virus. The replication and pathogenicity of the rescued viruses (rHLJ09SH01 and rHLJ09SH01A205) were investigated. Compared to rHLJ09SH01A205, rHLJ09SH01 showed a moderate growth advantage in vitro and in vivo, in addition to exhibiting a higher oncogenicity rate and lethality rate in layers and broilers. Increased vascular endothelial growth factor A (VEGF-A) and vascular endothelial growth receptor subtype 2 (VEGFR-2) expression was induced by rHLJ09SH01 more so than by rHLJ09SH01A205 during early embryonic vascular development, but this increased expression disappeared when the expression levels were normalized to the viral levels. This finding suggests that the expression of VEGF-A and VEGFR-2 is associated with viral replication and may also represent a novel molecular mechanism underlying the oncogenic potential of ALV-J. Overall, our findings not only indicate that the unique 205-nucleotide deletion in the ALV-J genome occurred naturally in China and contributes to increased pathogenicity but also point to the possible mechanism of ALV-J-induced oncogenicity.
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