# Infection with bovine leukemia virus belonging to group A or B-1 contributes more strongly to the development of enzootic bovine leukosis in young cattle than the presence of bovine lymphocyte antigen-DRB3 susceptibility alleles

**Authors:** Yuki Fujii, Masaki Maezawa, Masataka Akagami, Junko Kawakami, Yuri Fujimoto, Hisashi Inokuma

PMC · DOI: 10.1007/s00705-024-06102-7 · 2024-08-01

## TL;DR

This study shows that infection with specific bovine leukemia virus strains is a stronger factor in young cattle developing a certain disease than genetic susceptibility.

## Contribution

The study reveals that BLV group A or B-1 infection is more influential than BoLA-DRB3 alleles in young cattle with enzootic bovine leukosis.

## Key findings

- BLV group A or B-1 infection was more frequent in young cattle with EBL.
- This effect was observed regardless of BoLA-DRB3 allele presence.
- Infection with these BLV strains contributes more strongly to EBL in young cattle.

## Abstract

In this study, we compared the effects of different bovine leukemia virus (BLV) strains and bovine lymphocyte antigen (BoLA)-DRB3 alleles in cattle with enzootic bovine leukosis (EBL) aged either <3 years or ≥3 years. The frequency of infection with BLV belonging to group A or B-1 in cattle aged <3 years with EBL was significantly higher than that in cattle aged ≥3 years, regardless of which BoLA-DRB3 allele was present. This suggests that infection with group A or B-1 BLV contributes more strongly to the development of EBL in young cattle than the presence of early-EBL-onset susceptibility BoLA-DRB3 alleles.

The online version contains supplementary material available at 10.1007/s00705-024-06102-7.

## Linked entities

- **Diseases:** enzootic bovine leukosis (MONDO:0025489)

## Full-text entities

- **Genes:** BOLA (MHC class I antigen clone 2) [NCBI Gene 751813] {aka BoLA-N}
- **Diseases:** EBL (MESH:D016583)
- **Species:** Bos taurus (bovine, species) [taxon 9913], Bovine leukemia virus (no rank) [taxon 11901]

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Source: https://tomesphere.com/paper/PMC11294373