S100A4/Mts-overexpressing mice exhibit thick elastic laminae and mild pulmonary arterial hypertension, which can progress to neointimal lesions and perivascular inflammation with age.
Researchers tested whether a vasculotropic virus (gammaherpesvirus 68) could induce these lesions, finding that infection led to significant inflammatory responses and elastin degradation in S100A4/Mts1 mice.
Further studies suggested that the presence of elastin peptides may enhance viral entry into the vessel wall, indicating that early viral interactions with vascular tissues play a crucial role in the severity of vascular pathology post-reactivation.