Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of photodynamic inactivation on experimental herpes simplex keratitis in rabbits was investigated using neutral red as a photosensitizing dye followed by exposure to light at 425nm. Combined dye application and light exposure early in the disease (two days following infection) reduced to a minimal extent the severity and duration of the acute epithelial infection. The effect on well-established keratitis (three days postinfection) was negligible as evaluated by clinical grading, viral recovery, and histopathological study. In initial experiments, it was found that the dye and light did not have any observable deleterious effect on intact corneas or cause any noticeable delay in healing of injured cornias. Further, when light or dye were utilized alone, neither changed the severity or duration of the keratitis. In vitro treatment of the virus with light and dye destroys its ability to produce experimental keratitis.
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PMID:Photodynamic inactivation in experimental herpetic keratitis. 113 87

Topical application of 9-beta-d-arabinofuranosylhypoxanthine 5'-monophosphate (ara-HxMP) significantly inhibited the development of keratitis induced by types 1 and 2 herpes simplex virus and vaccinia virus in the eyes of rabbits. Parameters for evaluation of efficacy were infectivity (corneal opacity, lesion size, and type), Draize (erythema, conjunctival swelling, and discharge), and reduction in titer of recoverable virus from the eye. When the relative efficacy of the related compounds 9-beta-d-arabinofuranosyladenine (ara-A), ara-A 5'-monophosphate (ara-AMP), and ara-Hx was determined against type 1 herpes simplex virus in a parallel experiment, the more water-soluble compounds (ara-HxMP, ara-AMP) were the most effective. The relative efficacy of ara-A was also determined against type 2 herpes and vaccinia virus-induced keratitis. Mortality in rabbits due to central nervous system involvement caused by types 1 and 2 herpes simplex virus was inhibited. Ara-HxMP was not discernibly toxic to the eye at concentrations of at least 20%; efficacy was still discernible with a 0.1% solution.
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PMID:Viral keratitis-inhibitory effect of 9-beta-D-arabinofuranosylhypoxanthine 5'-monophosphate. 119 Jul 53

Bonaphthone (6-naphthoquinone-1,2) administered per os produces a prounced therapeutic effect in experimental herpetic keratitis of rabbits, induced by the virus of herpes simplex. With the topical appllication of bonaphthone in the form of an ointment the drug also produces a curative action in herpetic keratitis of rabbits. Combined application of bonaphthone locally and enterally in dealing with herpes in rabbits also acts beneficially, the same as its separate use.
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PMID:[Chemotherapeutic activity of bonafton in experimental herpetic keratitis in rabbits]. 122 24

Herpes simplex keratitis was found to be a common ophthalmic problem in Tunisia. Dendritic and geographic ulcers were complicated by deep stromal keratitis in 31% of patients, two thirds of whom were known to have been treated previously with corticosteroids. Herpes simplex virus was isolated from 41% of patients from whom corneal material was cultured. To develop an effective program for management of epithelial herpes in developing countries, treatment with idoxuridine was compared with debridement and patching. Average healing time for 31 ulcers treated with idoxuridine was 13 days, with three treatment failures; average healing time for 20 ulcers treated with debridement and patching was five days, with one failure. Debridement and patching of herpetic ulcers was an efficient way to treat herpes simplex keratitis within the context of overall medical care in Tunisia.
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PMID:Herpes simplex keratitis in a developing country. Natural history and treatment of epithelial ulcers in Tunisia. 126 38

Patients with active herpetic epithelial keratitis who had toxic reactions or were resistant to idoxuridine received vidarabine. Only one of 35 cases of herpetic epithelial keratitis without stromal disease failed to heal. Of 21 patients with active epithelial keratitis complicating stromal keratitis or uveitis. 11 had complete reepithelialization by day 14. Two patients were removed from the trial as treatment failures. The remaining cases healed in 21 to 48 days. In most instances the stromal keratitis was inactivated when the epithelial ulcer healed. In our patients treated with vidarabine, healing of herpes simplex epithelial ulcers was biphasic: Stage 1, progression from an active to an inactive viral ulcer, and Stage 2, complete reepithelialization.
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PMID:Vidarabine therapy of complicated herpes simplex keratitis. 127 44

We examined immunofluorescent staining and corneal sensitivity in 25 control subjects (25 eyes) with normal corneas, six patients (eight eyes) with possible herpes simplex keratitis, and 44 patients (48 eyes) with corneal lesions (recurrent erosion, superficial punctate keratitis, marginal ulcer, and follicular keratoconjunctivitis) in whom herpes simplex keratitis was not suspected. On immunofluorescent staining, all 25 control subjects had negative reactions, all eight eyes suspected of having herpes simplex keratitis had positive reactions, and 11 (23%) of the 48 eyes not suspected of having herpes simplex keratitis had positive reactions; the remaining 37 eyes had negative reactions. Of the 11 eyes not suspected of having herpes simplex keratitis but that had positive reactions on immunofluorescent staining, nine had recurrent erosions and the remaining two eyes had superficial punctate keratitis. Of the eight eyes with possible herpes simplex keratitis, seven (88%) had decreased corneal sensitivity. Of the 11 eyes not suspected of having herpes simplex keratitis but that had positive reactions on immunofluorescent staining, eight (73%) had decreased corneal sensitivity. Of the 37 eyes not suspected of having herpes simplex keratitis that had negative reactions on immunofluorescent staining, 11 (30%) had decreased corneal sensitivity.
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PMID:Immunofluorescent staining and corneal sensitivity in patients suspected of having herpes simplex keratitis. 131 74

Passive administration of antibody against herpes simplex virus type 1 (HSV-1) has been shown to protect against stromal keratitis and death from encephalitis. Although the exact mechanism by which passively-transferred antibody protects is not known, one of the features of protection by passively-transferred antibody is interference with the ability of the virus to spread within the nervous system. In the experiments reported herein, studies were performed to determine if 8D2, a monoclonal antibody against a type-common epitope of glycoprotein D, could protect mice from retinal necrosis following uniocular anterior chamber inoculation of HSV-1. Mice were protected from retinal necrosis when the antibody was administered 2 hours before virus inoculation or 24 hours after virus inoculation. When antibody was injected 2 hours before virus inoculation, the titer of virus at day 1 p.i. in the injected eyes of antibody-treated and control mice was the same, but by 3 days p.i., the titer of virus in the antibody-treated mice was significantly lower than that recovered from control mice. The titers of virus in the brains and in the uninoculated eyes of antibody-treated mice were also significantly lower than in control mice. The results of these studies suggest that passively-transferred antibody protects against retinal necrosis by limiting spread of virus to the CNS or replication of virus within the CNS.
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PMID:Protection from retinal necrosis by passive transfer of monoclonal antibody specific for herpes simplex virus glycoprotein D. 131 51

We analyzed the differentiation of two strains isolated from the conjunctiva and rhinorrhea of a patient with herpetic keratitis by the restriction endonuclease digestion method of herpes simplex virus (HSV) DNA. As a result two strains were identified as the same one. This result suggests that HSV contained in tears flows into the nasal cavity via the lacrimal canaliculi.
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PMID:Transmission of herpes simplex virus infection via lacrimal canaliculi. 131 37

We tested whether excimer laser photorefractive and phototherapeutic keratectomy may reactivate latent herpes simplex and cause recurrent keratitis in mice. Two of ten latently infected mice that were treated with ten excimer laser pulses to the corneal epithelium shed herpes simplex virus type 1, as did four of ten mice that were treated with 50 excimer laser pulses. Ocular shedding of herpes simplex virus was detected in four of ten mice that were treated with ethylenediamine-tetraacetic acid (EDTA) scraping of the corneal epithelium without laser keratectomy, and in six of ten mice on which combined EDTA-facilitated epithelial removal was performed followed by the application of ten excimer laser pulses. In both EDTA-treated groups, viral shedding was prolonged and 18 of 20 mice developed marked corneal opacification or neovascularization, or both. Corneal photoablation with the excimer laser may induce reactivation of latent herpes simplex virus, even in mice with clear and smooth-appearing corneas, and should be considered in the differential diagnosis of humans with persistent corneal epithelial defects after refractive or therapeutic excimer procedures.
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PMID:Reactivation of latent herpes simplex virus by excimer laser photokeratectomy. 132 Mar 29

Recurrences of herpetic stromal keratitis are believed to be initiated by reactivation of herpes simplex virus infection, probably in the trigeminal ganglion. Genetic features of the virus and the host as well as the immune status of the host influence the outcome of infection. Following infection on the snout with HSV-1, mice with normal corneas usually develop mild anterior segment disease. We studied the induction of herpetic infection in mice that had abnormal corneas, containing center due to trauma or a spontaneous dystrophy. The corneal abnormality led to more frequent herpetic stromal keratitis and more severe anterior chamber reaction. In addition, we found that snout-infected mice with dystrophic corneas had an increased risk of dying from viral infection. Our data suggest that not only the strain of virus and the genetic background of the mouse, but also the state of the cornea itself, can contribute to susceptibility to ocular herpes infection.
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PMID:Presence of Langerhans cells in the central cornea linked to the development of ocular herpes in mice. 132 20


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