# A GTPV-Based Murine Model Recapitulating Key Features of Lumpy Skin Disease for Preclinical Vaccine Evaluation

## TL;DR

Researchers developed a mouse model using a related virus to study lumpy skin disease, enabling faster and cheaper vaccine testing before using cattle.

## Contribution

A novel murine model using goatpox virus to mimic lumpy skin disease in mice for preclinical vaccine evaluation.

## Key findings

- Intranasal GTPV infection in mice caused weight loss, fever, and lung pathology similar to natural LSDV infection.
- Mice developed strong humoral and cellular immune responses, including IgM, IgG, and cytokine production.
- The model supports accelerated vaccine development by replicating key features of LSDV pathogenesis and immunity.

## Abstract

Lumpy skin disease poses a major threat to cattle farming, causing severe sickness and financial loss globally. A major obstacle to stopping this virus is that using cattle for every experiment is too expensive and complex, yet there have been no suitable lab animals to use instead. To address this, our research created a new way to study the disease using mice. We used a closely related goat virus as a substitute to mimic the infection. We found that delivering this virus into the nose caused the mice to lose weight and develop lung inflammation, closely mirroring the natural disease process. Importantly, the mice produced a strong immune response similar to what is seen in cattle. This confirms that our mouse model is a reliable tool for initial testing. It offers scientists a faster, cheaper method to screen potential vaccines before moving to livestock trials.

The global spread of lumpy skin disease (LSD), a devastating cattle disease caused by the lumpy skin disease virus (LSDV), is hampered by the lack of a practical small animal model for vaccine evaluation. Here, we established a mouse model by challenging C57BL/6 mice with goatpox virus (GTPV), a close relative of LSDV. Intranasal inoculation with a high dose (104.5 TCID50) of GTPV induced robust infection characterized by weight loss, fever, high viral loads in the lungs and livers, and significant pulmonary pathology including immune cell infiltration and alveolar wall thickening. Infected mice mounted potent humoral immunity, with rapid IgM and sustained IgG and GTPV-specific binding antibody responses. The infection also elicited a dynamic cellular immune response, marked by biphasic IFN-γ production and dose-dependent increases in IL-17A and TNF-α. This GTPV-based murine model effectively recapitulates critical aspects of LSDV pathogenesis and immunity, providing a valuable and accessible tool for the accelerated development and preclinical assessment of novel LSDV vaccines.