# Host transcriptome profiling for resistance against lumpy skin disease (LSD)

## TL;DR

This study explores gene expression differences in cattle to understand why some are more resistant to lumpy skin disease than others.

## Contribution

The study identifies IL1RAP gene expression as a potential determinant of resistance to lumpy skin disease in cattle.

## Key findings

- IL1RAP gene expression differs significantly between resilient and susceptible cattle before and after LSDV infection.
- Seven days post-infection may be a critical time point for LSD infection in cattle.
- Gene Ontology and KEGG pathway analyses highlight IL1RAP's involvement in LSD response.

## Abstract

Lumpy skin disease (LSD) is an acute or subacute systemic viral disease of cattle that shows variation in the response of cattle to LSD virus infection. To better understand the mechanisms underlying this response diversity in field studies and under carefully controlled artificial infections, we studied the differentially expressed genes (DEGs) between two resilient versus three susceptible Holstein bulls before an infection challenge and three time points after that.

The host transcriptome profiling revealed that IL1RAP gene expression could be a potential determinant in distinguishing between resilient and susceptible cattle (padj < 0.05). It was significantly shifted from up-regulated prior to infection to down-regulated three days post-infection in the LSD-resilient cattle. Its expression remained up-regulated among the susceptible cattle post-infection compared to pre-infection. The results showed that seven days post-infection may be a critical time point for LSD infection. The Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment test showed a few enriched GO terms and pathways relevant to the LSD and the involvement of the IL1RAP gene. This pilot study, with limited statistical power, is the first to investigate bovine gene expression profiling in response to LSDV.

The online version contains supplementary material available at 10.1186/s13104-025-07388-9.