Inflammatory and neuropathological responses to Vesiculovirus carajas encephalitis in adult mice: variability, tolerance and resistance

TL;DR

This study explores how Vesiculovirus carajas causes encephalitis in mice, focusing on inflammation and immune responses in the brain.

Contribution

The study reveals novel inflammatory and neuropathological features of CARV encephalitis in mice and suggests a unique neuroinvasion route.

Findings

CARV antigens were detected in necrotic neurons with microglial activation near blood vessels and ventricles.

Infected mice showed elevated brain cytokine levels, indicating a strong inflammatory response by day 10 post-infection.

The findings suggest CARV uses a hematogenous route for neuroinvasion, differing from other vesiculovirus species.

Abstract

Vesiculovirus carajas (CARV) is a pathogen with neuroinvasive potential, yet its impact on neuroinflammation and sickness behavior remains poorly understood. In this study, we investigated the neuropathological and immunological responses to CARV encephalitis in adult BALB/c mice. Mice were intranasally inoculated with either infected or uninfected brain homogenates, and clinical, histopathological, and cytokine profiles were analyzed. CARV antigens were primarily detected in necrotic neurons, with prominent microglial activation near the ventricles and blood vessels. By day 10 post-infection, infected mice exhibited significantly elevated levels of MCP-1, IFN-γ, IL-12 p70, TNF-α, IL-6, and IL-10 in the brain, indicating a strong inflammatory response. These findings highlight the inflammatory modulation associated with CARV infection and suggest a hematogenous route of neuroinvasion, distinguishing CARV from other vesiculovirus species. This study provides new insights into the pathogenesis of CARV encephalitis and its potential impact on neuroimmune dynamics.

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