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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence for latent infection of ocular tissues following topical corneal inoculation with herpes simplex virus type 1 (HSV) was sought in three strains of inbred mice that differ in susceptibility to HSV stromal keratitis. Corneas of BALB/c, C57BL/6, and DBA/2 mice were inoculated topically with HSV. At 6-8 weeks after inoculation, when no active ocular infection was present, minced whole eyes and trigeminal ganglia were assayed for latent virus. Virus was recovered by explantation from minced eyes of all three strains (DBA/2 = 20%; BALB/c = 17%; C57BL/6 = 7%). In order to determine which ocular structures harbored virus, corneas, retinas and choroid-sclera were cultivated separately. Virus was activated from corneas of DBA/2 and BALB/c mice, but not from corneas of C57BL/6 mice. These findings suggest that HSV is capable of establishing latent infection in ocular tissue of inbred mice and that the rate of establishment of latency is under host genetic control. Since neural cell bodies are not present in the cornea, the data suggest that latency is established in cells other than neurons.
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PMID:Recovery of herpes simplex virus from ocular tissues of latently infected inbred mice. 282 65

The spread of herpes simplex virus (HSV) through neural tissues was studied in three inbred mouse strains that differ in susceptibility to HSV stromal keratitis. The left eyes of BALB/c, C57BL/6, and DBA/2 mice were inoculated topically with HSV type 1. The optic and trigeminal nerves, trigeminal ganglia, and eyes were assayed for infectious virus on days 1, 2, 3, 4, 7, 9, 11 and 14 after inoculation. At 2-4 months post-inoculation, eyes and trigeminal ganglia were assayed for latent virus. Up to 7 days post-inoculation, infectious virus was present at a similar frequency in the inoculated eyes of mice from all three strains. The quantity of virus recovered, however, was mouse strain-dependent: DBA mice yielded the most virus; C57BL/6, the least. The frequency of virus recovery and the quantity of virus recovered from trigeminal nerves and ganglia also varied according to mouse strain. Infectious virus was recovered from the uninoculated right eye of some DBA and C57BL/6 mice 1 wk after inoculation. The overall incidence of latency differed among inbred mouse strains. However, in mice that developed ocular disease (blepharitis, dendritic keratitis, or stromal keratitis), there was no host strain-related difference in the incidence of latency. These results support the hypothesis that host genetic factors play a role in controlling HSV replication and the spread of virus to neural tissues after ocular HSV inoculation. This control may influence the development and severity of disease. However, once infection occurs, latency is established in both susceptible and resistant mouse strains.
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PMID:Spread of HSV and establishment of latency after corneal infection in inbred mice. 300 Sep 75

Corneal opacities were observed in numerous strains and stocks of laboratory mice (Mus musculus) from different microbiological environments. The opacities were characterized as acute and chronic inflammatory lesions of the corneal epithelium and anterior corneal stroma, including corneal ulcers and erosions, acute keratitis, stromal neovascularization and mineralization of the basement membrane zone. Some strains and stocks of mice from barrier-reared colonies had a high incidence of corneal opacities [DBA/2 (29.1%), C3H (16.2%), CF1 (16.2%) and BALB/c (10.0%)] while others had a lower incidence [CD-1 (4.3%) and C57BL/6 (4.1%)]. Axenic and gnotobiotic mice had a very low incidence of corneal opacities (1.6%). An experimental study demonstrated that twice weekly cage cleaning would reduce the incidence of corneal opacities to a very low level. A bacterial product, such as ammonia, is proposed as a significant factor in the pathogenesis of spontaneous corneal opacities in laboratory mice.
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PMID:Spontaneous corneal opacities in laboratory mice. 372 49

The corneas of four inbred strains of mice (BALB/c, DBA/2, C3H and C57BL/6) were inoculated with the RE strain of herpes simplex virus, type 1. The corneas were examined at frequent intervals and graded on a scale of 0 (clear cornea) to +5 (severe necrotizing stromal keratitis). At 3 weeks postinfection, the mean corneal scores were: DBA/2, 4.0; BALB/c, 2.2; C3H, 0.7; and C57BL/6, 0.15. The differences between the scores are statistically significant (P less than 0.05), except for the C3H and C57BL/6 strains. The order of severity of corneal disease in these mice corresponds to the order of susceptibility to systemic infection found in these same inbred strains. Additional studies of herpetic keratitis in inbred mice should prove helpful in understanding the genetic and immunologic basis of herpetic stromal keratitis.
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PMID:Herpetic keratitis in inbred mice. 648 Feb 98

Effects of a ragweed extract and ultraviolet (UV) radiation on Moraxella bovis-induced keratitis of DBA/2J mice were investigated. Mouse eyes were exposed to ragweed extract and/or UV radiation during induction of keratitis. Pathogenesis was enhanced by exposure to ragweed extract alone and by exposure to UV radiation alone. It was enhanced most when eyes were exposed to ragweed extract and UV radiation.
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PMID:Enhancement of Moraxella bovis-induced keratitis of mice by exposure of the eye to ultraviolet radiation and ragweed extract. 688 76

Both viral and host genetics affect the outcome of herpes simplex virus type 1 (HSV-1) infection in humans and experimental models. Little is known about specific host gene variants and molecular networks that influence herpetic disease progression, severity, and episodic reactivation. To identify such host gene variants we have initiated a forward genetic analysis using the expanded family of BXD strains, all derived from crosses between C57BL/6J and DBA/2J strains of mice. One parent is highly resistant and one highly susceptible to HSV-1. Both strains have also been fully sequenced, greatly facilitating the search for genetic modifiers that contribute to differences in HSV-1 infection. We monitored diverse disease phenotypes following infection with HSV-1 strain 17syn+ including percent mortality (herpes simplex encephalitis, HSE), body weight loss, severity of herpetic stromal keratitis (HSK), spleen weight, serum neutralizing antibody titers, and viral titers in tear films in BXD strains. A significant quantitative trait locus (QTL) on chromosome (Chr) 16 was found to associate with both percent mortality and HSK severity. Importantly, this QTL maps close to a human QTL and the gene proposed to be associated with the frequency of recurrent herpetic labialis (cold sores). This suggests that a single host locus may influence these seemingly diverse HSV-1 pathogenic phenotypes by as yet unknown mechanisms. Additional suggestive QTLs for percent mortality were identified--one on Chr X that is epistatically associated with that on Chr 16. As would be anticipated the Chr 16 QTL also modulated weight loss, reaching significance in females. A second significant QTL for maximum weight loss in male and female mice was mapped to Chr 12. To our knowledge this is the first report of a host genetic locus that modulates the severity of both herpetic disease in the nervous system and herpetic stromal keratitis.
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PMID:A forward phenotypically driven unbiased genetic analysis of host genes that moderate herpes simplex virus virulence and stromal keratitis in mice. 2465 95