# Construction and Biological Characterization of ORF133-Deletion Mutant of Lumpy Skin Disease Virus

## TL;DR

Researchers deleted a unique gene in the Lumpy Skin Disease Virus to study its role in viral replication and host adaptation.

## Contribution

The study introduces a recombinant virus with a deleted ORF133 gene and mouse antibodies to investigate its role in LSDV.

## Key findings

- ORF133 deletion affects viral replication in LSDV.
- Mouse polyclonal antibodies against ORF133 were successfully generated.
- The ORF133-deleted recombinant virus was constructed using homologous recombination.

## Abstract

Lumpy skin disease virus (LSDV), a Capripoxvirus genus member, causes severe cattle disease. Though Capripoxviruses share high nucleotide sequence homology indicating common ancestry, they have evolved distinct host adaptations. The LSDV genome encodes numerous proteins, with ORF133 being LSDV-specific and lacking clear homologs in other Capripoxviruses, implying potential roles in host range and virulence. To explore ORF133’s function, this study generated mouse polyclonal antibodies against ORF133 and constructed the ORF133-deleted recombinant virus (LSDVΔORF133-EGFP) via homologous recombination with an EGFP reporter. Preliminary characterization showed that ORF133 deletion affects viral replication. This study provides critical tools and theoretical references for subsequent investigations into the functional mechanisms underlying ORF133 in LSDV.