The role of herpes simplex virus secreted glycoproteins in herpetic keratitis

Smeraglia, R.; Hochadel, James F.; Varnell, Emily D.; Kaufman, Herbert E.; Centifanto-Fitzgerald, Y M

doi:10.1016/0014-4835(82)90042-2

Cited by 16 publications

(7 citation statements)

References 24 publications

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“…This secre tion of the truncated gC may be partly responsible for the induction of HSK in TN-l-inoculated mice. Smeraglia et al [8] reported that HSV-1 strains which induced HSK secreted larger amounts of glycoproteins than the viruses which in duced epithelial disease and no HSK and that gC was the major constituent of the secreted proteins.…”

Section: Discussionmentioning

confidence: 99%

“…The gC is a major envelope glycoprotein of HSV-1 and was present on the cell surface infected with ev ery clinical HSV-1 isolate previously examined [2], HSV-l-induced stromal keratitis (HSK) is reported to be mediated by the T cell response to HSV-1 in the corneal stro ma [3], and gC is a dominant antigen in the induction of the host T cell response [4,5]. In the previous study, a gC-negative mutant of HSV-1, gC-39, showed a highly reduced path ogenicity [6] and was a poor inducer of T cell response and HSK in mice [7], Another study suggested that the HSKproducing viruses of HSV-1 secreted larger amounts of gly coproteins including gC than the epithelial-disease-produc ing viruses [8]. TN strains exhibit a gC-negative phenotype, that is, TN virions and infected cells did not express gC on their surface [9].…”

Section: Introductionmentioning

confidence: 99%

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Stromal Keratitis Induced by a Unique Clinical Isolate of Herpes simplex Virus Type 1

et al. 1994

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Glycoprotein C (gC)-negative clinical isolates of herpes simplex virus type 1 (HSV-1) are very rare. An HSV-1 strain (TN-1), isolated from a patient with her-petic keratitis, exhibited a gC-negative phenotype. While a gC-negative mutant showed reduced pathogenicity and failed to induce herpetic stromal keratitis (HSK) in a previously reported mouse model, TN-1 induced HSK in mice comparable to RTN-1–20–3, a gC-positive recombinant virus derived from TN-1. Virus growth in eyes and brains and the mortality of TN-1-inoculated mice were equal to or higher than those of RTN-1–20–3-inoculated mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Stromal Keratitis Induced by a Unique Clinical Isolate of Herpes simplex Virus Type 1

et al. 1994

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“…Clinical isolates from patients with stromal disease maintained this characteristic upon repeated cell culture passages (16). More recently Smeraglia et al (22) demonstrated that the capacity to induce stromal disease in rabbits was related to increased production of HSV-1 glycoproteins. In this regard, it is noteworthy that HSV-1 (Sh) has been found to induce abundant glycopeptide synthesis (3).…”

Section: Discussionmentioning

confidence: 95%

The pathogenesis of herpetic ocular disease in the Guinea pig

Wander

Bubel

McDowell

1987

Archives of Virology

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A detailed study of the pathogenesis of herpetic eye disease in the guinea pig was undertaken to further develop this animal model. Several well-known HSV-1 strains were tested for their ability to produce disease and cause acute and latent infections of the trigeminal ganglion: McKrae, KOS, McIntyre, RE, and Shealey. Two HSV-2 strains failed to cause eye infections. The Shealey strain [HSV-1 (Sh)] produced the most severe eye infections, characterized by epithelial and stromal disease, corneal vascularization and ulcerative blepharitis. Consequently, HSV-1 (Sh) was selected as the prototype strain for this study. The frequency and severity of HSV-1 (Sh) eye disease patterns was determined by a semi-quantitative rating scale, which permitted accurate monitoring of the temporal development of the disease patterns cited above. Virus shedding from infected eyes was also quantified. All of the HSV-1 strains tested established trigeminal ganglionic latency with varying frequency, although HSV-1 (Sh) latency approached 100 percent. The kinetics of acute ganglionic infection by HSV-1 (Sh) was determined, and peak virus titers occurred on the third day after corneal inoculation. This study emphasizes the usefulness of the Guinea pig model for investigations on the pathogenesis, prevention and treatment of herpetic eye infections.

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“…It has been demonstrated that both CD4' and CD8+ T cells may be involved with the relative extent of participation dependent upon the host and the virus strain (Hendricks & Tumpey, 1990;Niemialtowski & Rouse 1992). It has been proposed that virus participates in the development of edema by deposition of viral antigen-antibody complexes within the stroma (Myers & Pettit 1973), by incorporation of viral glycoproteins into host cell membranes leading to an autoimmune-like response (Centifanto-Fitzgerald et al 1982), and by secretion of viral glycoproteins in a soluble antigenic form causing a neutrophilic response (Centifanto-Fitzgerald et al 1982;Smeraglia et al 1982). Inhibition of any of these events could account for the more favorable results obtained following addition of corticosteroid to the therapeutic regimen.…”

Section: Discussionmentioning

confidence: 99%

Herpetic stromal disease: Response to acyclovir/steroid therapy

O’Brien

Segundo

Guy

et al. 1996

Acta Ophthalmologica Scandinavica

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The efficacy of combined acyclovir and steroid therapy in the treatment of herpetic stromal disease was evaluated by clinical evaluation of disease, the rebound of disease following termination of therapy, and the recovery of virus and viral DNA from corneas in a rabbit model. Therapy with acyclovir alone produced a significant reduction in corneal thickness in 10% of eyes. Addition of steroid to acyclovir therapy decreased the severity of stromal disease as measured by corneal thickness and increased the frequency of response to treatment to 63% of eyes. All eyes receiving acyclovir alone experienced rebound of disease following termination of therapy. Combined therapy increased the severity of rebound of corneal disease. Virus was recovered from cell cultures established after recovery from rebound in 50% of untreated and treated eyes. Viral DNA was detected by PCR in five of the nine corneal cultures which did not produce infectious virus.

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The role of herpes simplex virus secreted glycoproteins in herpetic keratitis

Cited by 16 publications

References 24 publications

Stromal Keratitis Induced by a Unique Clinical Isolate of Herpes simplex Virus Type 1

Stromal Keratitis Induced by a Unique Clinical Isolate of Herpes simplex Virus Type 1

The pathogenesis of herpetic ocular disease in the Guinea pig

Herpetic stromal disease: Response to acyclovir/steroid therapy

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