Host-Strain-Specific Responses to Pneumonia Virus of Mice Infection: A Study of Lesions, Viral Load, and Cytokine Expression

TL;DR

This study examines how different mouse strains respond to a virus that causes lung disease, showing that both the virus and immune response affect the severity of illness.

Contribution

The study reveals host-genetic influences on viral pathogenicity and cytokine-driven disease progression in a mouse model.

Findings

Viral load correlates with microscopic lesions across multiple mouse strains.

Cytokine levels are linked to lesion severity in 129/Sv and BALB/c mice.

Genetic background significantly affects disease outcomes in PVM-infected mice.

Abstract

Pneumonia virus of mice (PVM) infection is a reference animal model for human respiratory syncytial virus (hRSV), a leading cause of lower respiratory tract disease in children under 5 years of age and in the elderly. This longitudinal study employed necropsy to examine macroscopic lesions, histological slides to assess microscopic lesions, and qRT-PCR to measure lung viral load and cytokine expression in PVM-infected mice from three different genetic backgrounds, spanning from day 1 to day 6 post-infection. Our analysis reveals a strong correlation between viral load and microscopic lesions across the 129/Sv, BALB/c, and SJL/J mouse lines, indicating that PVM pathogenicity is partially driven by the virus itself. Additionally, a significant correlation between cytokine levels and lesion severity was observed in 129/Sv and BALB/c mice, suggesting an important role of cytokines in disease progression. This study emphasizes the interplay between viral load and cytokine-driven tissue damage, with genetic background significantly influencing disease outcomes.

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