ArticleVeterinary research2018
A chicken liver cell line efficiently supports the replication of ALV-J possibly through its high level viral receptor and efficient protein expression system.
Article in Veterinary research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Heterogeneous CRISPR/Cas9 Editing ofInternational journal of molecular sciences · 2026Article
- Hepatocyte production across embryonic stages in chicken: an in vitro approach.BMC veterinary research · 2025Article
- Reduced aggregation of the leghorn male hepatoma cell line in suspension by supplementing dextran sulfate in the media.Animal bioscience · 2025Article
- Q221K mutation in VP2 drives antigenic shift of infectious bursal disease virus.Frontiers in immunology · 2025Article
- Chicken hepatomegaly and splenomegaly associated with novel subgroup J avian leukosis virus infection.BMC veterinary research · 2022Article
- The tyrosine phosphatase SHP-2 dephosphorylated by ALV-J via its Env efficiently promotes ALV-J replication.Virulence · 2021Article
- Gp37 Regulates the Pathogenesis of Avian Leukosis Virus Subgroup J via Its C Terminus.Journal of virology · 2020Article
- Co-infection of vvMDV with multiple subgroups of avian leukosis viruses in indigenous chicken flocks in China.BMC veterinary research · 2019Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we identified a chicken liver cell line (LMH) which could strongly support the replication of ALV-J (Subgroup J of avian leukosis virus) with high viral titer. Notably, ALV-J was efficiently detected by ELISA in LMH cells 1 day before DF1 cells. In comparison with DF1 cells, LMH cells not only expressed higher levels of ALV-J receptor chNHE-1, but also possessed a more efficient protein expression system for foreign genes. Thus, LMH cells could be a novel tool to shorten the ALV-J eradication approach and accelerate studies on the pathogenesis and oncogenesis of ALV-J.
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