Abstract
Feline immunodeficiency virus infection of cats provides a model to elucidate mechanisms of lentiviral pathogenesis. We isolated a non-domestic FIV from a Pallas' cat, FIV-Oma, which replicates in feline PBMCs and CRFK cells. To gain insights into FIV pathogenesis, we compared rates of viral replication and apoptosis of FIV-Oma with FIV-PPR in the MYA-1 T-cell line. To minimize heterogeneity of virus, infections were initiated with virus derived from molecular clones. Viral DNA and RNA levels, assessed by qPCR and qRT-PCR, apoptosis, and supernatant reverse transcriptase were slower in FIV-Oma infections. Immunostaining for cellular Gag showed that few cells were productively infected. The majority of cells infected with either virus instead became apoptotic. Apoptosis was detectable within 6 h PI, suggesting activation of a signaling pathway. We propose that apoptosis is due to interaction of virus with cells, and is the usual outcome of infection by cytopathic FIVs in these cells.
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