FELINE IMMUNODEFICIENCY VIRUS DECREASES CELL-CELL COMMUNICATION AND MITOCHONDRIAL-MEMBRANE POTENTIAL

The in vitro effects of viral replication on mitochondrial membrane po tential (MMP) and gap junctional intercellular communication (GJIC) we re evaluated as two parameters of potential cellular injury. Two disti nct cell types were infected with the Petaluma strain of feline immuno deficiency virus (FIV). Primary astroglia supported acute FIV infectio n, resulting in syncytia within 3 days of infection, whereas immortali zed Crandell feline kidney (CRFK) cells of epithelial origin supported persistent FIV infection in the absence of an obvious cytopathic effe ct. An examination of cells under conditions that included an infectio n rate of more than 90% for either population revealed that the astrog lia produced about four times more virus than the CRFK cells. The mito chondrial uptake of the cationic fluorescent dye rhodamine 123 in infe cted astroglia was less than 45% of that of normal control cells, wher eas the MMP of the CRFK cells, which produced about one-fourth as much virus, was 80.8% of that of the normal cells. Cell-cell communication between adjacent cells was determined by the recovery of fluorescence following photobleaching of a single cell. In spite of the lower leve l of innate cell-cell communication among cultured CRFK cells than amo ng astroglia, viral replication resulted in a 30% decrease in the GJIC of both astroglia and CRFK cells. These studies indicate that cell in jury, as defined by an inhibition of MMP and GJIC, tan occur as a resu lt of persistent and acute infection with the Petaluma strain of FIV.