<i>Herpesvirus hominis</i>
            : Isolation from Human Trigeminal Ganglion

Bastian, Frank O.; Rabson, Alan S.; Yee, Carole; Tralka, Tommie Sue

doi:10.1126/science.178.4058.306

Cited by 355 publications

(112 citation statements)

References 9 publications

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“…However, HSV-1 establishes latency in the sensory neurons that supply the infected areas. The primary host cells for HSV-1 latency are the sensory neurons of the trigeminal ganglia (Bastian et al, 1972). During HSV-1 latency in neurons, the only significantly expressed viral RNA is the latency associated transcript (LAT) (Stevens, 1978).…”

Section: Introductionmentioning

confidence: 99%

Two alphaherpesvirus latency-associated gene products influence calcitonin gene-related peptide levels in rat trigeminal neurons

Hamza

Higgins

Ruyechan

2007

Neurobiology of Disease

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Herpes simplex virus type-1 (HSV-1) initially infects mucoepithelial tissues of the eye and the orofacial region. Subsequently, the virus is retrogradely transported through the axons of the trigeminal sensory neurons. HSV-1 establishes a life-long latent infection in these neurons, during which the transcription of the viral genome is silent, except for the sequences encoding the latency associated transcript (LAT). To determine if HSV-1 latency might affect calcitonin gene-related peptide (CGRP) expression in trigeminal sensory neurons, we transfected primary neuronal cultures of trigeminal ganglia from rat embryos with plasmids expressing LAT. In the presence of Bone Morphogenetic Protein-7 (BMP7), CGRP was expressed in 49% of sensory neurons. However, this percentage was reduced to 19% in neurons transfected with LAT expressing plasmids. We also found that transfection of the IE63 gene of varicella-zoster virus (VZV) reduced the percentage of trigeminal neurons containing CGRP. However, the observed effect of IE63 in contrast to that of LAT, was completely reversed by treatment of cultures with MgCl 2 , which indicates that the effect of IE63 was due to increased release of CGRP from trigeminal neurons. We provide here the first evidence that HSV-1 LAT decreases the level of CGRP in trigeminal neurons. These effects may be important for reducing the neuroinflammatory response, thus protecting host neuronal cells during HSV-1 latency in trigeminal neurons. In contrast, increased release of CGRP in the presence of IE63 protein may contribute to the neuralgias associated with VZV infection.

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Section: Introductionmentioning

confidence: 99%

Two alphaherpesvirus latency-associated gene products influence calcitonin gene-related peptide levels in rat trigeminal neurons

Hamza

Higgins

Ruyechan

2007

Neurobiology of Disease

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“…Herpes simplex virus type 1 (HSV-1) may be isolated from herpetic facial lesions , some head sensory ganglia (Bastian et al, 1972;Baringer & Swoveland, 1973;Baringer, 1974;Warren et al, 1978), brain of herpes encephalitis cases (Longson & Bailey, 1977;Koskiniemi & Vaheri, 1982), genital regions in a minority of herpes genitalis cases (Peutherer & Smith, 1981 ;Chang, 1977), and herpetic infections at other anatomical locations (e.g. Buss & Schary3, 1979).…”

Section: Introductionmentioning

confidence: 99%

Variable Restriction Endonuclease Sites of Herpes Simplex Virus Type 1 Isolates from Encephalitic, Facial and Genital Lesions and Ganglia

Chaney¹,

Warren

Subak‐Sharpe³

1983

Journal of General Virology

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SUMMARYThe distribution of restriction endonuclease (RE) sites was compared for 84 herpes simplex virus type 1 (HSV-1) isolates obtained from the ganglia, facial lesions, genital lesions and from brain tissue from herpes encephalitis cases. The isolates came from Canada, the U.K., the U.S.A. and Japan. Out of a total of 224 sites identified, 87 were variable. Three of the 30 most variable sites were at significantly (P < 0-05) different frequencies in groups of isolates from distinct anatomical sites of isolation; one of these, and a further two sites, were at significantly different frequencies in groups from distinct geographical origins. There are at least two inter-related linkage groups. However, most of the site combinations appear to be random. The variability of RE sites in contiguous genome segments, which include both non-coding and coding sequences, show a marked heterogeneity, indicating that some viral gene sequences are more variable than others. The three RE sites at different frequencies in viral groups from distinct anatomical sites of isolation are in two genome segments : map units 27 to 35 and 50 to 57. We infer from the observed associations with anatomical site of viral isolation that part of at least one of these segments may modulate viral virulence in man following infection.

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“…Indeed, HSV establishes latency in neurons that depend on NGF and incubation with NGF and epidermal growth factor delays HSV reactivation [13][14][15][16][17]. Moreover, blocking of NGF with antibodies or depletion of NGF results in HSV reactivation in vitro, ex vivo and in animal models [17][18][19][20][21][22][23].…”

Section: /3mentioning

confidence: 99%

Herpes Simplex Virus and Neurotrophic Factors

VB¹

2015

JHVRV

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Herpesvirus hominis : Isolation from Human Trigeminal Ganglion

Cited by 355 publications

References 9 publications

Two alphaherpesvirus latency-associated gene products influence calcitonin gene-related peptide levels in rat trigeminal neurons

Two alphaherpesvirus latency-associated gene products influence calcitonin gene-related peptide levels in rat trigeminal neurons

Variable Restriction Endonuclease Sites of Herpes Simplex Virus Type 1 Isolates from Encephalitic, Facial and Genital Lesions and Ganglia

Herpes Simplex Virus and Neurotrophic Factors

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