Expression of herpes simplex virus type 2 latency-associated transcript in neurons and nonneurons.

The presence of herpes simplex virus type 2 (HSV-2) transcription during in vivo latent infection was investigated by in situ hybridization. Latent infection of mouse dorsal root ganglion was investigated with the BamHI p fragment of HSV-2, which resulted in evidence of ganglion hybridization, and other fragments representing approximately 40% of the genome, which did not result in hybridization. Strand specificity of hybridization was investigated in studies with synthetic oligonucleotides, which supported the conclusion that a latency-associated transcript(s) had been detected. Hybridization was detected with oligonucleotides complementary to the infected-cell polypeptide 0 (ICP0) template strand but not with oligonucleotides synthesized from the ICP0 template strand. Although most hybridization occurred over neurons, in some instances hybridization appeared to occur over nonneuronal ganglion cells, and this was more evident when tissue sections were examined by phase contrast microscopy. Although these results supported the usual neuronal site of HSV-2 latency, latency in nonneuronal cells may be important in considering the pathobiology of HSV-2 infections.