Volume 76 (2026) Issue: 2026 No#1

TNF-α gene variants and receptor expression associated with BLV infection in Colombian Holstein cattle

Author(s): Cristina Úsuga-Monroy, Albeiro López-Herrera

Keywords:Cytokine, dairy herds, gene expression, SNP, proviral load.

Bovine leukemia virus (BLV) is a single-stranded RNA retrovirus whose persistence in infected cattle indicates that innate immune responses, particularly antiviral cytokines, are insufficient to control infection. Tumor necrosis factor alpha (TNF-α) is a key proinflammatory cytokine that may contribute to antiviral defense, acting through two membrane-bound receptors: TNF-α receptor I (TNF-α RI) and TNF-α receptor II (TNF-α RII). Both receptors participate in apoptotic and immune-regulatory pathways. This study aimed to investigate the – 824 A/G polymorphism in the promoter region of the TNF-α gene and to quantify TNF-α RI and TNF-α RII transcript levels, assessing their association with proviral load and persistent lymphocytosis (PL) in Holstein cattle. Blood samples from 140 cows were analyzed for TNF-α genotypes and receptor mRNA expression. Data were normalized and analyzed using one-way analysis of variance (ANOVA) to assess differences in gene expression among the experimental groups. The TNF-α G/G genotype was significantly associated with increased odds of BLV infection (p=0.006). TNF-αRI mRNA expression differed significantly between BLV-positive and BLV-negative cows (p=0.0017), whereas TNF-αRII expression showed no differences according to infection status (p=0.999). In BLV-negative animals, TNF-αRI and TNF-αRII expression levels differed significantly, with lower RII expression (p<0.0001); this pattern was not observed in infected cows, regardless of aleukemic or persistent lymphocytosis status. Aleukemic cows exhibited reduced RI and RII expression compared with RI levels in uninfected animals (p<0.05). No significant correlations were detected between TNF-αRI or TNF-αRII expression and PBMC counts or proviral load in infected cattle (ρ≤|0.23|; p>0.05). The results indicate an association between TNF-α genetic variation, receptor expression patterns, and BLV infection status, suggesting that TNF-α signaling may contribute to the host–virus interaction during BLV infection. Further longitudinal and functional studies are required to clarify the biological mechanisms linking TNF-α regulatory polymorphisms with viral persistence and disease progression.