Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript
GC Perng, C Jones, J Ciacci-Zanella, M Stone… - Science, 2000 - science.org
GC Perng, C Jones, J Ciacci-Zanella, M Stone, G Henderson, A Yukht, SM Slanina…
Science, 2000•science.orgLatent infections with periodic reactivation are a common outcome after acute infection with
many viruses. The latency-associated transcript (LAT) gene is required for wild-type
reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain
unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT− virus but not
with LAT+ viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells.
Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.
many viruses. The latency-associated transcript (LAT) gene is required for wild-type
reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain
unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT− virus but not
with LAT+ viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells.
Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.
Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. The latency-associated transcript (LAT) gene is required for wild-type reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT −virus but not with LAT + viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells. Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.
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