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

Richard Tenser, W. A. Edris, K. A. Hay, B. E. De Galan

Research output: Contribution to journalComment/debate

10 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2745-2750
Number of pages6
JournalJournal of Virology
Volume65
Issue number5
StatePublished - Jan 1 1991

Fingerprint

Human herpesvirus 2
Virus Latency
Human Herpesvirus 2
hybridization
neurons
Oligonucleotides
Neurons
oligonucleotides
Ganglia
Phase-Contrast Microscopy
Peptides
polypeptides
Spinal Ganglia
Virus Diseases
Infection
infection
cells
In Situ Hybridization
Genome
in situ hybridization

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Cite this

Tenser, Richard ; Edris, W. A. ; Hay, K. A. ; De Galan, B. E. / Expression of herpes simplex virus type 2 latency-associated transcript in neurons and nonneurons. In: Journal of Virology. 1991 ; Vol. 65, No. 5. pp. 2745-2750.
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abstract = "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.",
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Expression of herpes simplex virus type 2 latency-associated transcript in neurons and nonneurons. / Tenser, Richard; Edris, W. A.; Hay, K. A.; De Galan, B. E.

In: Journal of Virology, Vol. 65, No. 5, 01.01.1991, p. 2745-2750.

Research output: Contribution to journalComment/debate

TY - JOUR

T1 - Expression of herpes simplex virus type 2 latency-associated transcript in neurons and nonneurons

AU - Tenser, Richard

AU - Edris, W. A.

AU - Hay, K. A.

AU - De Galan, B. E.

PY - 1991/1/1

Y1 - 1991/1/1

N2 - 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.

AB - 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.

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VL - 65

SP - 2745

EP - 2750

JO - Journal of Virology

JF - Journal of Virology

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