Early pathological changes in the central nervous system of acutely feline-immunodeficiency-virus-infected cats.

Abstract

The animal model of feline immunodeficiency virus (FIV) infection of cats was used to dissect the pathogenic role of microglia within the first 6 months of infection. Applying real-time PCR, microglia-associated FIV replication was first detectable at 14 days past inoculation (dpi) and remained at elevated levels throughout the whole observation period. In contrast, FIV RNA levels within paired serum samples declined again after an initial peak between 14 dpi and 28 dpi. Concomitant with the onset of viral reproduction, microglia transiently upregulated expression of MHC class I and class II molecules. Virus-induced microglial activation was followed by a mild infiltration of peripheral leukocytes into the CNS parenchyma. The presented data suggest that microglia is infected by FIV very early after peripheral entry of the virus. Virus replicating microglia withstands eradication by brain-infiltrating leukocytes resulting in formation of a brain-resident virus reservoir, which probably cannot be cleared by peripheral chemotherapy.