Isolation of Herpes Simplex Virus From Human Trigeminal Ganglia, Including Ganglia From One Patient With Multiple Sclerosis

Warren, K. G.; Gilden, D. H.; Brown, Stuart A.; Devlin, Mary; Wróblewska, Zofia; Subak‐Sharpe, J. H.; Koprowski, Hilary

doi:10.1016/s0140-6736(77)92501-6

Cited by 91 publications

(40 citation statements)

References 5 publications

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“…This gene expression occurred under the control of the LAT promoter during the latent phase of this virus. Like HSV, known to become latent in the sensory ganglia, [19][20][21][22][23] this chimeric HSV-1 may enter the latent phase in the anterior horn motor neurons with expression of ␤-gal activity after transport from the skeletal muscle. The spread of ␤-gal activity in the spinal cord did not further progress later than 14 days after inoculation.…”

Section: Discussionmentioning

confidence: 99%

Long-term gene expression in the anterior horn motor neurons after intramuscular inoculation of a live herpes simplex virus vector

et al. 2000

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To clarify the feasibility of the herpes simplex virus (HSV) vector in expressing the foreign gene in the motor neuron, we inoculated a live attenuated HSV expressing ␤-galactosidase (␤-gal) activity under a latency-associated transcript promoter in the right gastrocnemius muscle of rats. Expression of ␤-gal activity was observed 5 days after inoculation in the bilateral anterior horn cells of the spinal cord that innervates the inoculation muscle. However, the spread of ␤-gal activity was not observed in the inoculation muscle. Without significant pathological changes, the spread of ␤-gal-expressing neurons was observed in the lumbosacral

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Section: Discussionmentioning

confidence: 99%

Long-term gene expression in the anterior horn motor neurons after intramuscular inoculation of a live herpes simplex virus vector

et al. 2000

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“…This gene expression occurred under the control of the LAT promoter during the latent phase of infection. Like HSV, known to become latent in the sensory ganglia, [26][27][28][29][30] this chimeric HSV-1 may enter the latent phase in the anterior horn motor neurons with expression of ␤-gal activity after transport from the skeletal muscle and interneuronal spread.…”

Section: Discussionmentioning

confidence: 99%

Effect of immunity on gene delivery into anterior horn motor neurons by live attenuated herpes simplex virus vector

et al. 2001

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“…During primary mucosal infection, the virus enters nerve endings and is transported by axonal transport to the sensory ganglia that innervate the face and oral mucosa; here the viral genome remains in a non-replicative, latent form for the life of the host. The trigeminal ganglion of the fifth cranial nerve is the most often reported site of HSV-1 latency in humans (Baringer & Swoveland, 1973;Bastian et al, 1972;Warren et al, 1977). Recurrent disease of the mouth (herpes labialis) or eye (herpes keratitis) is believed to occur when the virus reactivates in the ganglion and travels down the branches of this nerve, resulting in a recrudescent peripheral infection with patho~nomonic lesions (Spruance, 1984;Kaufman, 1978).…”

Section: Introductionmentioning

confidence: 99%

Oral-oesophageal inoculation of mice with herpes simplex virus type 1 causes latent infection of the vagal sensory ganglia (nodose ganglia)

Gesser

Vályi-Nagy

Altschuler

et al. 1994

Journal of General Virology

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Herpes simplex virus type 1 (HSV-1) gingivostomatitis during childhood is known to result in a latent infection of the trigeminal ganglion neurons, which innervate the oral mucosa. During latency the viral genome is maintained in a non-infectious state. However, stimuli such as stress, fever or localized trauma can cause HSV-1 to reactivate in neurons and produce recrudescent disease in the peripheral tissues. Recently, HSV-1 proteins and nucleic acids have been detected in biopsies from human duodenal and gastric ulcers, raising the possibility that HSV-1 latency within the enteric nervous system is involved in this chronic recurrent gastrointestinal disorder. The studies in mice described here were done to determine whether HSV-1 latency could be established in neurons that innervate the murine gut. We found that after either intraperitoneal or oral-oesophageal inoculation of mice, HSV-1 establishes a latent infection in nodose ganglia of the vagus nerve, whose sensory neurons project to the gastrointestinal tract. This animal model of HSV-1 latency in the vagal sensory ganglia will be useful to examine the possible relationship between HSV-1 and recurrent gastrointestinal disease.

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Isolation of Herpes Simplex Virus From Human Trigeminal Ganglia, Including Ganglia From One Patient With Multiple Sclerosis

Cited by 91 publications

References 5 publications

Long-term gene expression in the anterior horn motor neurons after intramuscular inoculation of a live herpes simplex virus vector

Long-term gene expression in the anterior horn motor neurons after intramuscular inoculation of a live herpes simplex virus vector

Effect of immunity on gene delivery into anterior horn motor neurons by live attenuated herpes simplex virus vector

Oral-oesophageal inoculation of mice with herpes simplex virus type 1 causes latent infection of the vagal sensory ganglia (nodose ganglia)

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