Differential chemokine induction by the @entity19 adenovirus type-1 in the central nervous system of susceptible and resistant strains of XXXX .

@entity12427 @entity8929 @entity548 @entity39 @entity19 @entity75 @entity22425 @entity638 @entity9701 @entity1188 @entity25880 @entity204 @entity15369
@entity19 adenovirus-type 1 (MAV-1) has recently been shown to cause a fatal hemorrhagic @entity75 in certain strains of @entity19 whereas other strains are resistant. Morbidity is associated with a productive infection of cerebrovascular endothelial cells, resulting in @entity39 of the vasculature, @entity1188 , @entity548 and @entity204 within 4 - 6 days. Previous studies were not able to define a role for the innate or acquired immune response. In the current study we have addressed the effect of MAV-1 on chemokine and chemokine receptor expression in the central nervous system (CNS) and spleen of susceptible (C57BL/6) and resistant (BALB/c) strains of @entity19 . Intra-peritoneal infection with MAV-1 in C57BL/6 animals resulted in early and prominent induction of @entity15369 / @entity15369 in the spleen and CNS. Increased expression of @entity8929 , @entity12427 , @entity22425 and @entity638 was also noted in the CNS of MAV-1-infected C57BL/6 animals commencing around 72 h post-infection. In contrast, chemokine expression in BALB/c animals was more restricted with prominent upregulation only of @entity9701 in the CNS. In situ hybridization identified the vascular endothelium and CNS glia as the principal site of @entity15369 / @entity15369 production in the C57BL/6 animals. The chemokine receptors @entity25880 -5 were upregulated in the CNS of both strains of @entity19 . These data show that productive infection of the CNS with MAV-1 leads to the upregulation of a characteristic pattern of chemokines and their receptors, which may point to a role for these factors in disease pathogenesis.
