Equine herpesvirus type 1 (EHV1) induces alterations in the immunophenotypic profile of equine monocyte-derived dendritic cells.
Authors: Claessen Christophe, De Lange Valérie, Huang Teng, Ma Guanggang, Osterrieder Nikolaus, Favoreel Herman, Van de Walle Gerlinde R
Journal: Veterinary journal (London, England : 1997)
Summary
# Editorial Summary: EHV1's Manipulation of Dendritic Cell Function Equine herpesvirus type 1 represents a persistent threat to equine health, yet the mechanisms by which it evades immune surveillance remain incompletely understood. Claessen and colleagues investigated how EHV1 infection alters the immunological profile of monocyte-derived dendritic cells (MDDC)—key orchestrators of immune responses—by examining changes in cell surface markers following viral exposure. The research revealed that EHV1 selectively downregulates several critical molecules on infected dendritic cells, including MHC class I, the maturation markers CD83 and CD86, the pattern recognition receptor CD206, and adhesion molecules CD29 and CD172a, whilst leaving MHC class II and other adhesion molecules intact. Notably, whilst the herpesviral VHS protein (virion host-shutoff) and pUL49.5 did not drive these changes, the viral protein pUL56 partially mediated CD83 and CD86 downregulation, suggesting EHV1 employs multiple and nuanced immune-evasion strategies. For equine professionals managing EHV1-affected horses, these findings underscore that viral persistence depends on sophisticated manipulation of dendritic cell function, which may inform future development of more effective vaccines or antiviral therapies that counter these specific immune-suppressive mechanisms.
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Practical Takeaways
- •EHV1 actively evades immune detection by suppressing dendritic cell activation markers, which may explain the virus's ability to establish persistent infections in horses
- •Understanding these immune evasion mechanisms could inform development of improved vaccines or immunotherapies for EHV1 prevention
- •The role of specific viral proteins (pUL56) in immune suppression provides potential targets for antiviral strategies
Key Findings
- •EHV1 infection of equine monocyte-derived dendritic cells induced down-regulation of MHCI, CD83, CD86, CD206, CD29 and CD172a surface proteins
- •CD83 and CD86 down-regulation was partially mediated by the viral protein pUL56
- •Down-regulation of these proteins was not mediated by virion host-shutoff (VHS) protein or pUL49.5
- •EHV1 employs multiple distinct mechanisms to suppress functionally important dendritic cell surface proteins involved in immune response