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 frequency of latent infection as established in trigeminal ganglia of rabbits, mice and hamsters with human herpesvirus type 1 (HVH) was compared using two different virus strains. Explantation proved to be effective in reisolation of HVH from ganglion tissue, which did not yield infectious virus at time of its removal. After healing of acute keratitis, the latent infection in homolateral gasseric ganglia of rabbits was detected at a relatively high frequency (60-80 per cent) up to 120 days post infection (p.i.) in case of both virus strains. The activation rate was a little lower in hamsters. After inoculation of suckling and young mice with a sublethal dose of HVH by oral and nasal routes, approximately 40-100 per cent of the animals had virus in their gasseric ganglia during the acute period; 30-60 days later only 10-25 per cent had virus in the latent form. Immunofluorescent and electron microscopic examination of the explanted ganglion tissue showed the presence of HVH in neurons, neuronal satellites and Schwann cells. The nuclei of noneural cells contained numerous crystalline arrays. The possibility that pseudounipolar neurons of the regional sensoric ganglion are not the exclusive site of HVH latency is discussed.
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PMID:Experimental latent herpesvirus infection in rabbits, mice and hamsters: ultrastructure of the virus activation in explanted gasseric ganglia. 23 93

Corneal intrastromal inoculation of guinea pigs with approximately 10(4) plaque-forming units of live, adapted varicella-zoster virus (VZV) resulted in reproducible, acute, superficial corneal disease in all animals. The culture-positive VZV ocular infection progressed to involve 30% to 40% of the corneal surface in a diffuse punctate keratitis and 10% to 15% of this surface with microdendrites, characteristic of VZV-induced ocular disease. Retrograde dissemination of VZV to the trigeminal ganglia, midbrain, cerebellum, and superior cervical ganglia was demonstrated by whole-cell coculture VZV recovery. Central nervous system VZV dissemination, manifested by transient neurologic symptoms and pneumonitis, was evident in 60% of the animals. Varicella-zoster virus spread to the trigeminal ganglion during acute and early-latent infection was evident by electron microscopy.
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PMID:Ocular varicella-zoster virus infection in the guinea pig. A new in vivo model. 254 23

Peptide-containing nerve fibers (peptidergic fibers) abundantly innervate the mammalian cornea. We investigated their role in ocular herpes simplex infection in mice by using capsaicin, which causes degeneration and permanent loss of peptidergic neurons in neonates and temporary peptide depletion in adult animals. The corneas of neonatally denervated BALB/c mice were observed for capsaicin-induced keratitis at 11-14 wk of age and were then infected bilaterally with herpes simplex virus 1 (HSV-1); trigeminal (TG) ganglia were cocultivated 6 wk later to establish the rate of latent infection. We also applied capsaicin eye drops to adult BALB/c mice that had been infected with HSV-1 6 wk earlier, and measured viral shedding before, and 3 days and 2 months after, administration of capsaicin drops; TG ganglia of these animals were cocultivated at 3 days and 2 months after capsaicin application. Neurotrophic keratitis was found in 81% of neonatally denervated animals; mortality rate due to HSV-1 infection was reduced from 80% in the controls to 24% in the capsaicin-treated group, and recovery of latent virus by cocultivation was reduced by 50%. Viral shedding could not be produced by capsaicin eye drops in adult animals infected with HSV-1. However, recovery of latent virus was significantly reduced in TG ganglia sampled 3 days and 2 months after capsaicin drops were instilled. Our findings suggest 1) that peptidergic fibers play a crucial role in the establishment of trigeminal HSV-1 latency and 2) that reactivation of latently infected ganglia can be inhibited by topical capsaicin.
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PMID:Role of peptidergic neurons in ocular herpes simplex infection in mice. 255 22

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

This study evaluated the continued presence of herpes simplex virus (HSV) nucleic acid sequences after resolution of acute herpetic stromal keratitis in the rabbit ocular model. Forty-four rabbits were inoculated bilaterally with 10(5) plaque-forming units of RE strain HSV-1 by intrastromal injection. All eyes were cultured for the presence of HSV during acute disease and immediately before the animals were killed. Full-thickness corneal buttons were then removed and processed for in situ hybridization with a 3H-labelled HSV DNA probe representing the full-length HSV genome. HSV nucleic acid sequences were detected autoradiographically at all time intervals examined. HSV nucleic acid sequences were localized in the epithelium and the anterior stromal keratocytes during acute disease and in all corneal layers during latent infection. Retention of HSV nucleic acid sequences, either HSV DNA or HSV RNA, or both, in corneal tissues (epithelium, stroma, and endothelium) may be a contributing factor in the development of HSV-induced stromal keratitis.
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PMID:Detection of HSV nucleic acid sequences in the cornea during acute and latent ocular disease. 284 36

Herpetic ocular disease is still one of the major causes of corneal blindness. Due to its unique morphological structure, the eye is one of the most studied organs--in both clinical and experimental models of herpetic infections. Herpes simplex virus (HSV) can react with human host cells to produce cytocidal infection, persistent infection, or latent infection. Whilst the establishment of viral latency in the sensory ganglia was demonstrated and extensively studied, recent evidences based on: (a) demonstration of viral particles by electron microscopy and of HSV positive antigen cells in human corneae with inactive stromal keratitis; (b) experimental animal and in vitro studies with the use of organ cultures, co-cultivation methods and molecular biology techniques; suggest the possibility of local latency in non-neural tissues as an additional source of dormant viruses that could reactivate and lead to local reinfection of the affected target organ. Reactivation of a herpetic infection may therefore require both the existence of a dormant herpetic reservoir in the ganglia, and a predilected target organ with possible independent mechanisms of local latency and reactivation. Possible mechanisms of triggers for reactivation of herpetic ocular disease are discussed.
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PMID:Herpetic imprint on privileged areas of its target organs: local latency and reactivation in herpetic keratitis. 285 57

Herpes simplex virus (HSV) was isolated from the corneal discs of six patients with herpes simplex keratitis, which were removed during penetrating keratoplasty and then cultured in vitro. The demonstration of persistent infection in stromal keratitis, even when the condition is quiescent, emphasizes the need for antiviral agents in treatment. The findings support the possibility that latent infection may become established at a peripheral site.
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PMID:Isolation of herpes simplex virus from corneal discs of patients with chronic stromal keratitis. 298 22

Complete gene synthesis methods have been used to construct analogs of human interferons (IFNs): these include a consensus of the known human IFN-alpha S, designated IFN-alpha Con1 and a variant of human IFN-gamma, designated IFN-gamma 4A. These interferons, in purified form, were used topically against herpes simplex virus type 1 (HSV-1) induced ocular keratitis in rabbits. Eyes pretreated with IFN-alpha Con1 had decreased signs of infection and a lower incidence of HSV-1 positive trigeminal ganglia (3 of 14 positive) compared to the placebo treated (10 of 14 positive). IFN-alpha Con1 was as effective as natural IFN-alpha subtypes on a units basis, despite the very high specific activity of this analog. IFN-gamma 4A used under similar conditions do not result in beneficial effects with treatments beginning 24 or 48 hr before or 4 hr after virus inoculation. Rabbits with confirmed latent HSV infection were treated topically with IFN-alpha Con1 (10(6) units per eye each day) either before or before and after attempts to intentionally reactivate the infection by bilateral iontophoresis of 6-hydroxydopamine plus topical epinephrine treatment of the corneas. These IFN-alpha Con1 treatment regimens along with intentional reactivation during latency did not: (1) lessen the frequency of inducible ocular shedding episodes; (2) alter the mean time of 3-5 days between attempts to reactive latent infection and the appearance of HSV in tears; or (3) significantly change the incidence of HSV-positive trigeminal ganglia (83-100% HSV positive).
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PMID:Human alpha and gamma interferon analogs in rabbits with herpetic keratitis. 392 22

Latent infection of the trigeminal ganglion following ocular and labial herpes simplex in the mouse was investigated. Latent infection of the ophthalmic part of the trigeminal ganglion followed subclinical ocular infection. When primary infection resulted in severe eye disease, latent infection was subsequently demonstrated not only in ophthalmic parts of the ganglion but also in parts which did not serve the eye. Primary infection of the lip resulted in latent infection of the mandibular part of the trigeminal ganglion, but also of maxillary and ophthalmic parts. Previous infection by herpes simplex virus in a non-ocular site necessitated a hundred-fold increase in the amount of virus required to initiate keratitis which resulted in a much lower incidence of latent infection and only in the ophthalmic part of the ganglion. The results are interpreted to explain how latent infection of the ophthalmic part may precede and provide a source of virus for symptomatic eye disease. Such latent infection is most likely to arise from previous subclinical ocular infection or primary infection in a non-ocular site.
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PMID:Ocular herpes simplex and the establishment of latent infection. 630 Nov 14

A 70 year-old-man with recurrent herpetic keratitis had a meningo-encephalitis with transient left hemiplegia and disorders of consciousness. EEG disclosed periodic slow waves on the right temporal region. Isotope and CT scans showed focal abnormalities in the same region. Antibodies to herpes simplex virus were demonstrated by complement fixation in serum and specific antiherpes IgG and IgM by immunofluorescence assay in serum and CSF. A year later the patient had a status epilepticus. CT scan showed a large right temporal hypodense area. CSF was abnormal with pleiocytosis, increased protein and IgG levels. High titers of antiherpes IgG persisted in serum and CSF. Neuropsychological tests did not demonstrate any memory impairment. The occurrence of persistent inflammation after herpes simplex encephalitis is discussed. The unusual benign course without antiviral therapy, may be related to the reactivation of a latent infection with an efficient immunological response. The unilateral temporal necrosis may explain the absence of amnestic sequelae.
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PMID:[Acute necrotizing herpetic encephalitis with a spontaneously improving clinical course]. 669 26


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