The pathogenesis of herpetic ocular disease in the Guinea pig

Wander, Arden H.; Bubel, H. Curt; McDowell, Shana

doi:10.1007/bf01310780

Cited by 13 publications

(6 citation statements)

References 17 publications

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“…Various studies in mouse models found that in acute infection, viral strains differ in terms of pathogenesis and pattern of neurovirulence and retinovirulence, and this may be due to differences in extent and direction of transport transneurally [21,22] . Wander et al studied numerous strains of HSV-1 and determined that different strains presented in various patterns of disease severity in the acute and latent infection [23,24]. A higher number of latent virus copies has been suggested to promote reactivation by overwhelming the cellular mechanisms that silence virus transcription [25].…”

Section: Primary Infectionmentioning

confidence: 99%

“…A higher number of latent virus copies has been suggested to promote reactivation by overwhelming the cellular mechanisms that silence virus transcription [25]. In guinea pigs, the Shealey strain produced the most severe acute eye infections, characterized by severe epithelial and stromal lesions, corneal neovascularization and ulcerative blepharitis; this strain also produced the highest load of latent viral DNA in the TG [23]. Viral strains such as 17 Syn+, McKrae and KOS/M latently infected similar numbers of mouse neurons, but the number of viral genome copies per neuron was significantly greater in the 17 Syn+ and McKrae strains than in KOS/M [26].…”

Section: Primary Infectionmentioning

confidence: 99%

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Ocular Herpes Simplex Virus: How are Latency, Reactivation, Recurrent Disease and Therapy Interrelated?

et al. 2011

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Most humans are infected with herpes simplex virus (HSV) type 1 in early childhood and remain latently infected throughout life. While most individuals have mild or no symptoms, some will develop destructive HSV keratitis. Ocular infection with HSV-1 and its associated sequelae account for the majority of corneal blindness in industrialized nations. Neuronal latency in the peripheral ganglia is established when transcription of the viral genome is repressed (silenced) except for the latency-associated transcripts and microRNAs. The functions of latency-associated transcripts have been investigated since 1987. Roles have been suggested relating to reactivation, establishment of latency, neuronal protection, antiapoptosis, apoptosis, virulence and asymptomatic shedding. Here, we review HSV-1 latent infections, reactivation, recurrent disease and antiviral therapies for the ocular HSV diseases.

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Section: Primary Infectionmentioning

confidence: 99%

Section: Primary Infectionmentioning

confidence: 99%

Ocular Herpes Simplex Virus: How are Latency, Reactivation, Recurrent Disease and Therapy Interrelated?

et al. 2011

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“…The total sIgA-positive rate was 36.59% (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26) in the patient group, whereas in the controls, no positive result was obtained among the cases. Figure 2 showed that the levels of specific sIgA were significantly higher in stromal keratitis than that in control group (P = 0.003).…”

Section: Resultsmentioning

confidence: 93%

Tear HSV-Specific Secretory IgA as a Potential Indicator for Recurrent Stromal Herpes Simplex Keratitis

Huang

Wang

Zhang

2013

Cornea

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“…Following intracorneal inoculation with HSV-1 in mice, rabbits, and guinea pigs, the incidence and severity of keratitis vary with different strains of virus (18,(64)(65)(66). The spectrum of disease can vary from mild or nonexistent to severe (18,(64)(65)(66). The dose of a particular strain of virus can also affect the incidence of disease (8,64).…”

Section: Discussionmentioning

confidence: 99%

“…These investigators used a different strain and dose of HSV-1 from those used in the experiments in the present study. Following intracorneal inoculation with HSV-1 in mice, rabbits, and guinea pigs, the incidence and severity of keratitis vary with different strains of virus (18,(64)(65)(66). The spectrum of disease can vary from mild or nonexistent to severe (18,(64)(65)(66).…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of Herpes Simplex Virus Type 1-Induced Corneal Inflammation in Perforin-Deficient Mice

Chang

Galle

Maggs

et al. 2000

J Virol

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Herpetic stromal keratitis (HSK) is an inflammatory disease of the cornea that often results in blindness.It is mediated by a host immune response which is triggered by herpes simplex virus (HSV) infection. Immune effector mechanisms are hypothesized to be important in disease development. We investigated, in a mouse model, whether perforin-dependent cytotoxicity is an important effector mechanism in the production of HSK. Wild-type (C57BL/6) and perforin-deficient (PKO) mice were infected intracorneally with HSV-1 strain F. Clinical disease and histologic lesions of the cornea at 23 days postinfection (p.i.) were significantly less severe in HSV-1-infected PKO mice than in infected wild-type mice. mRNA for the chemokine macrophage inflammatory protein 1␣ (MIP-1␣) was detected by reverse transcription-PCR in the corneas of infected wild-type mice but not in the corneas of infected PKO mice at 23 days p.i. Adoptive transfer of wild-type HSV-1 immune T-cell-enriched splenocytes into HSV-1-infected PKO mice restored the disease phenotype which was seen in infected wild-type mice. In contrast, mice carrying a null-function mutation in the Fas ligand, which is involved in an alternative cytotoxic mechanism, developed clinical disease and histologic lesions which were comparable to those in wild-type mice. Viral clearance from the eyes of PKO mice was not impaired. There was no significant difference between the infectious viral titers isolated from the eyes of PKO and wild-type mice. Our findings show that perforin is important in the pathogenesis of HSK.Herpetic stromal keratitis (HSK) is a chronic inflammation of the cornea which is a consequence of infection by herpes simplex virus (HSV). It is the main nontraumatic cause of corneal blindness in people in developed countries (54). HSV-1-induced corneal inflammation in the mouse model is an immunopathological condition mediated by T lymphocytes (11, 20-22, 38, 48, 49, 54). T-cell-deficient mice, such as athymic nude mice, scid mice, or thymectomized mice, do not develop keratitis following intracorneal infection with HSV-1. However, these mice develop HSK upon intracorneal HSV-1 infection if they have previously received an adoptive transfer of HSV-1 immune T lymphocytes (3,11,12,21,37,43,58).The main effector mechanisms mediated by T lymphocytes are the secretion of soluble factors such as cytokines and chemokines and the lysis of target cells. Cytokines, such as gamma interferon, have been proposed as mediators of HSK (2,20,24). However, studies of gamma interferon knockout mice failed to demonstrate a role for gamma interferon in the pathogenesis of HSV-induced stromal keratitis (5). Chemokines have also been postulated to be involved in the development of HSK (55, 57, 59). There is evidence that macrophage inflammatory protein 1␣ (MIP-1␣), a beta chemokine involved in lymphocyte recruitment, plays a role in the development of HSK (60).Immune cytotoxic effector mechanisms play a role in the development of many immune-mediated disorders. The two main cytotoxic ef...

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The pathogenesis of herpetic ocular disease in the Guinea pig

Cited by 13 publications

References 17 publications

Ocular Herpes Simplex Virus: How are Latency, Reactivation, Recurrent Disease and Therapy Interrelated?

Ocular Herpes Simplex Virus: How are Latency, Reactivation, Recurrent Disease and Therapy Interrelated?

Tear HSV-Specific Secretory IgA as a Potential Indicator for Recurrent Stromal Herpes Simplex Keratitis

Pathogenesis of Herpes Simplex Virus Type 1-Induced Corneal Inflammation in Perforin-Deficient Mice

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