Recovery of herpes-simplex virus from human trigeminal ganglions

Baringer, J. Richard; Swoveland, Peggy

doi:10.1097/00006534-197309000-00032

Cited by 73 publications

(85 citation statements)

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“…Gene delivery to neurons and glia should also be reduced to some extent because of neutralizing antibodies to HSV-1, which have been detected in 40-90% of humans. 12,13 Injection into an intracranial tumor and into normal brain are comparable in the following ways: (1) the injection of the vector will cause some tissue damage and influx of serum and will thus allow neutralizing antibodies to come in contact with the vector; and (2) when a recombinant HSV virus is used as the vector (or the helper virus in an HSV amplicon system), viral gene expression is likely to occur and elicit a cellular immune response against infected cells. However, herpes amplicon vectors can also be produced in a helper virus-free system, 37 in which case there is no de novo synthesis of HSV proteins after infection.…”

Section: Discussionmentioning

confidence: 99%

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Pre-existing herpes simplex virus 1 (HSV-1) immunity decreases, but does not abolish, gene transfer to experimental brain tumors by a HSV-1 vector

et al. 1998

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Section: Discussionmentioning

confidence: 99%

“…12,13 The humoral and cellular immune response in pre-exposed patients could prove an obstacle for HSV-1-mediated gene transfer. Neutralizing antibodies could block the initial infection of target cells and the cellular immune reponse could lead to premature elimination of infected cells, thus reducing the number of transduced cells.…”

Section: Introductionmentioning

confidence: 99%

Pre-existing herpes simplex virus 1 (HSV-1) immunity decreases, but does not abolish, gene transfer to experimental brain tumors by a HSV-1 vector

et al. 1998

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“…The trigeminal ganglia of a significant proportion of human cadavers harbour latent virus (Baringer & Swoveland, 1973). In addition, recurrent infections have been shown to be due to re-expression of endogenous virus.…”

Section: Introductionmentioning

confidence: 99%

Recurrence Phenotypes and Establishment of Latency Following Rabbit Keratitis Produced by Multiple Herpes Simplex Virus Strains

Gerdes

Smith

1983

Journal of General Virology

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SUMMARYDistinct high frequency recurrence (HFRc) or low frequency recurrence (LFRc) phenotypes were observed following rabbit keratitis with three type 1 and five type 2 herpes simplex virus strains. LFRc strains were found to have latently infected the animal but were detected very rarely, if at all, in the eye following the acute phase. The recurrence phenotypes defined in singly infected animals remained unchanged following bilateral infection of the same animal with strains of opposite phenotype. Cocultivation of virus from bilaterally infected animals showed that both virus strains were capable of latently infecting the same animal. Restriction enzyme analysis of plaque-purified virus revealed that some ganglia were latently infected with both parental strains, Recombinants were also found. Some latently infected animals could be re-infected acutely. However, establishment of latency by the superinfecting strain was inhibited.

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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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Recovery of herpes-simplex virus from human trigeminal ganglions

Cited by 73 publications

References 0 publications

Pre-existing herpes simplex virus 1 (HSV-1) immunity decreases, but does not abolish, gene transfer to experimental brain tumors by a HSV-1 vector

Pre-existing herpes simplex virus 1 (HSV-1) immunity decreases, but does not abolish, gene transfer to experimental brain tumors by a HSV-1 vector

Recurrence Phenotypes and Establishment of Latency Following Rabbit Keratitis Produced by Multiple Herpes Simplex Virus Strains

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

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