# Research Progress on Pathogenesis and Prevention of Avian Leukosis Virus J Subgroup (ALV-J)

**Authors:** Xinyu Liu, Xi Lan

PMC · DOI: 10.3390/vetsci13020152 · Veterinary Sciences · 2026-02-04

## TL;DR

This review explains how Avian Leukosis Virus J affects chickens, causes disease, and how researchers are working to prevent it through breeding and gene editing.

## Contribution

The paper provides a comprehensive review of recent advances in understanding ALV-J pathogenesis and prevention strategies, including gene editing.

## Key findings

- ALV-J causes cancer-like diseases in chickens, leading to economic losses in poultry farming.
- CRISPR-Cas9 gene editing is a promising strategy for developing disease-resistant chickens.
- Viral evolution in the env gene and LTR regions contributes to immune evasion and host range expansion.

## Abstract

Avian leukosis virus subgroup J is a contagious virus that causes cancer-like diseases in chickens and has become a serious problem for poultry farming worldwide. Since it was first discovered, this virus has spread from meat-type chickens to egg-laying and local chicken breeds, leading to major economic losses due to reduced productivity and increased mortality. This review aims to clearly explain how the virus infects chickens, how it causes disease, and why it is difficult to control. We summarize recent research showing that some chickens naturally carry genes that make them more resistant to infection, and scientists are using this knowledge to develop disease-resistant chickens through selective breeding and modern gene-editing methods. The review also discusses how the virus can weaken the immune system, evolve rapidly, and sometimes escape control measures, which makes prevention challenging. In addition, we highlight progress and remaining gaps in developing faster diagnostic tools, safer vaccines, and effective farm-level control strategies. Finally, we emphasize the importance of long-term monitoring systems and clean breeding programs to stop the virus from spreading between generations. Overall, this work helps farmers, researchers, and policymakers better understand this disease and supports the development of healthier poultry populations, safer food production, and more sustainable agricultural practices that benefit society as a whole.

As a major retrovirus threatening global poultry farming, Avian Leukosis Virus Subgroup J (ALV-J) has expanded its host range since discovery, extending from conventional broilers to layer chickens and native breeds. Its diverse oncogenic manifestations, including myeloid leukemia, hemangiomas, and tumors of immune and visceral organs, have led to increased mortality, reduced productivity, and substantial economic losses in the poultry industry. Based on the current body of literature, this review summarizes and synthesizes advances in the etiological characteristics, infection and pathogenic mechanisms, host resistance, and research progress in prevention and control of ALV-J. Accumulating evidence indicates that viral evolution driven by mutations and recombination—particularly in the env gene and LTR regions—plays a central role in host range expansion, tumor diversity, and immune evasion. Current studies consistently demonstrate that host resistance to ALV-J is a multifactorial process involving genetic polymorphism, innate immune responses, and cellular autonomous defense systems. In this context, recent advances in disease-resistant breeding highlight CRISPR-Cas9-mediated gene editing as a promising strategy for blocking viral entry or replication. Despite these advances, major gaps remain, including an incomplete understanding of virus–host interaction networks, limited insight into co-infection-mediated synergistic pathogenicity, the absence of effective vaccines, and insufficient large-scale epidemiological surveillance and purification systems. Addressing these challenges will be critical for the development of integrated prevention strategies and the sustainable control of ALV-J in poultry production.

## Linked entities

- **Genes:** ERVW-1 (endogenous retrovirus group W member 1, envelope) [NCBI Gene 30816], ltr (loiterer) [NCBI Gene 10216629]
- **Diseases:** Avian Leukosis (MONDO:0025381), myeloid leukemia (MONDO:0004643)

## Full-text entities

- **Genes:** CCND1 (cyclin D1) [NCBI Gene 396341], DCLK1 (doublecortin like kinase 1) [NCBI Gene 418903], TLR7 (toll like receptor 7) [NCBI Gene 418638] {aka chTLR7}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 396282] {aka BCL-2, PCKBCL2}, IRF7 (interferon regulatory factor 7) [NCBI Gene 396330] {aka IRF3, cIRF-3}, MIR23B (microRNA 23b) [NCBI Gene 777877] {aka MIRN23B, gga-mir-23b, mir-23b}, IRF1 (interferon regulatory factor 1) [NCBI Gene 396384], NCKAP1 (NCK associated protein 1) [NCBI Gene 424000], MYC (v-myc avian myelocytomatosis viral oncogene homolog) [NCBI Gene 420332] {aka c-myc}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, MIR375 (microRNA 375) [NCBI Gene 777903] {aka MIRN375, gga-mir-375, mir-375}, SLC9A1 (solute carrier family 9 member A1) [NCBI Gene 419580], CTNNB1 (catenin beta 1) [NCBI Gene 395964] {aka CHBCAT, beta-catenin}, IFNA3 (interferon) [NCBI Gene 396398] {aka IFN-alpha, IFN-gamma, IFNA, IFNA1, IFNA2, IFNA6}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 424467], VEGFA (vascular endothelial growth factor A) [NCBI Gene 395909] {aka VEGF}, TERT (telomerase reverse transcriptase) [NCBI Gene 420972] {aka chTERT}, TET2 (tet methylcytosine dioxygenase 2) [NCBI Gene 422540], LOC107052719 (uncharacterized LOC107052719) [NCBI Gene 107052719] {aka SE21Q1b, gag}, IFIH1 (interferon induced with helicase C domain 1) [NCBI Gene 424185] {aka MDA5, chMDA5}, MIR125B2 (microRNA 125b-2) [NCBI Gene 777929] {aka MIR125B, MIR125B-2, MIRN125B, gga-mir-125b, gga-mir-125b-2, mir-125b-2}, CD320 (CD320 molecule) [NCBI Gene 420066] {aka TVA}
- **Diseases:** neoplasms of the liver, spleen, and kidneys (MESH:D013160), myeloid leukaemia (MESH:D015458), neoplasms of myeloid cells (MESH:D018307), necrosis (MESH:D009336), angiomas (MESH:D006391), liver tumors (MESH:D008113), infectious disease (MESH:D003141), Co (MESH:D060085), death (MESH:D003643), viral (MESH:D014777), Infection (MESH:D007239), bleeding (MESH:D006470), tumorigenesis (MESH:D063646), Newcastle Disease (MESH:D009521), injury to (MESH:D014947), Avian Influenza (MESH:D005585), myeloid leukemia (MESH:D007951), myeloma (MESH:D009101), hepatosplenomegaly (MESH:C535727), ALV infection (MESH:D001353), Tumor (MESH:D009369)
- **Chemicals:** m6A (MESH:C005955), CO2 (MESH:D002245), lipid (MESH:D008055), ALV-J (-), N6-methyladenosine (MESH:C010223)
- **Species:** Newcastle Disease Virus [taxon 11176], Gallus gallus (bantam, species) [taxon 9031], Gallid alphaherpesvirus 2 (Marek disease virus type 1, no rank) [taxon 10390], Reticuloendotheliosis virus (no rank) [taxon 11636], Avian leukosis virus ev/J (no rank) [taxon 1401444], Adenoviridae (family) [taxon 10508], Homo sapiens (human, species) [taxon 9606], Rous sarcoma virus (no rank) [taxon 11886], Arthrospira sp. LV (species) [taxon 2231211], Avian leukosis virus (no rank) [taxon 11864]
- **Mutations:** W38A, N123I, A to E, E39A, A-E, E39
- **Cell lines:** DF-1 — Gallus gallus (Chicken), Spontaneously immortalized cell line (CVCL_XF08)

## Full text

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## Figures

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## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945213/full.md

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Source: https://tomesphere.com/paper/PMC12945213