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)

Our study was designed to investigate the mechanism of the stromal reaction in experimental ocular infection of murine eyes with herpes simplex virus (HSV). Severe stromal keratitis with scarring occurred in BALB/c mice after infection of the scarified cornea but similar reactions did not occur in athymic mice. However, if athymic mice were given adoptive transfers of lymphoid cells, a severe necrotizing and ulcerative keratitis accompanied by scarring resulted. The lesion progressed more quickly in recipients of lymphoid cells specifically immune to HSV and containing cytotoxic T-lymphocyte activity. In such mice, necrosis and ulceration were marked on the sixth day after transfer compared with 9-12 days for those given nonimmune cells. Removal of T-lymphocytes from the immune lymphoid population by treatment with specific antiserum and complement abrogated the adoptive transfer of the stromal reaction. Our results further demonstrate that stromal keratitis represents a host immunopathologic response to HSV infection in which T-lymphocytes are essential participants. Multiple mechanisms of T-cell immunopathology appear to be operating, including a reaction mediated by cytotoxic T-lymphocytes.
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PMID:Role of T-lymphocytes in the pathogenesis of herpetic stromal keratitis. 661 24

Two immunocompromised patients with herpetic geometric glossitis, a clinically distinctive form of lingual herpes simplex virus (HSV) type 1 infection, are described. The significant features of herpetic geometric glossitis are summarized, the clinical differential diagnosis of this form of HSV infection is reviewed, and the possible pathogenesis of these lingual lesions is discussed. Both of our patients, as well as all previously described patients with this condition, had extremely painful cross-hatched, branched, and/or linear fissures on the dorsal aspect of the tongue. Symptoms promptly resolved within 1 to 2 days, and the fissures subsequently healed within 3 to 12 days after systemic acyclovir therapy was initiated. In contrast to tongue lesions of herpetic geometric glossitis, similar-appearing lingual lesions of other conditions are usually asymptomatic. The similar morphology of corneal dendrites in herpetic epithelial keratitis and linear fissures in herpetic geometric glossitis suggest the possibility that these HSV mucosal lesions may have a common pathogenesis.
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PMID:Herpetic geometric glossitis: a distinctive pattern of lingual herpes simplex virus infection. 750 16

In a retrospective study we evaluated 49 consecutive penetrating keratoplasties for herpes simplex keratitis. Mean follow-up was 44.2 months. Survival analysis with Kaplan-Meier curve showed an overall survival rate (clear graft) of 88% at one year, 76% at two years and 72% at four years postoperatively. Survival analysis showed a recurrence-free survival rate of 72% at one year, 59% at two years and 51% at four years postoperatively. Of the 13 non-primary graft failures, 9 happened in eyes with an HSV recurrence. Recurrence of HSV infection occurred in 18 (39%) eyes at an average of 12.6 months after surgery (range 0.3-46). Five (28%) of the recurrences occurred within two months after the start of steroid treatment for rejection. Nine (50%) of the recurrences cases resulted in a clouded graft at the end of follow-up. 73% of the eyes with a clear graft had a VA of 0.25 or better. We conclude from these data that a recurrence of a herpetic infection following corneal transplantation is the main reason for graft failure in this group.
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PMID:Recurrent herpetic keratitis in penetrating keratoplasty. 854 40

A novel multiplex nested polymerase chain reaction (PCR) assay was designed and evaluated for routine diagnosis of herpes simplex virus (HSV) infections in patients with either putative HSV infection of the central nervous system or suspected HSV keratitis. Single-tube amplification of HSV type 1 (HSV-1) or type 2 (HSV-2) DNA extracted from cerebrospinal fluid (CSF) or from keratectomy specimens was followed by differentiation of the virus type-specific PCR products either by agarose gel analysis or by DNA enzyme immunoassay. Among 417 CSF specimens obtained from 395 consecutive patients with clinically suspected HSV infection, 11 (2.6%) were positive for HSV-1 DNA and four (1.0%) probes were positive for HSV-2 DNA. None of the specimens was positive for both HSV-1 and HSV-2 DNA. The genome of HSV-2 was detected in a CSF sample obtained from a woman with meningoencephalitis and genital herpes. The presence of PCR inhibitors was detected in six of 111 (5.4%) reconstructed CSF samples. Inhibition could be removed following extraction with a commercial kit. HSV-1 DNA, but no HSV-2 DNA, was detected in corneal buttons obtained from patients with suspected herpetic keratitis. No contamination has been recorded during the 2-year routine use of this test, which has met the specific requirements of a diagnostic laboratory.
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PMID:Suitability and clinical application of a multiplex nested PCR assay for the diagnosis of herpes simplex virus infections. 889 44

Herpes viruses are among the most prevalent of human virus infections. Productive replication of herpes simplex virus (HSV) is usually confined to mucocutaneous sites by the rapid deployment of innate and adaptive immune responses. Infection invariably results in establishment of latency and in some cases results in periodic reactivation of the virus. This article focuses primarily on ocular herpes with emphasis on the pathogenesis of stromal keratitis. Herpetic stromal keratitis (HSK) is an immunopathologic disease, which indeed is one of the leading causes of blindness in the Western world. The mechanisms by which HSV infection in human beings results in HSK is not well understood but studies using the mouse model has clearly indicated the role of T-cell-mediated immune response as the cause for ocular damage. We, in this article, attempt to provide an interpretive synthesis on different aspects of HSK pathogenesis, reviewing what is currently known and speculating on mysterious issues, such as, whether HSK represents a virus-induced autoimmune disease. We also discuss aspects of remission of the disease.
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PMID:Immunopathogenesis of herpetic ocular disease. 943 61

Drug-resistance of herpes simplex virus (HSV) is caused most frequently by mutation of the viral thymidine kinase (TK) gene. To elucidate the significance of detecting nucleotide changes of the TK gene for screening drug-resistant viruses, the frequency and variation of the genetic polymorphisms in the whole coding region of the TK gene were studied in 14 acyclovir-susceptible HSV type 1 (HSV-1) clinical isolates from 14 patients with epithelial herpetic keratitis. Two reference HSV-1 laboratory strains, McKrae and PH, and two acyclovir-resistant variants of the PH strain were also studied as controls. Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing detected nucleotide differences at 24 positions, and amino acid substitutions at 12 codons in the TK gene of the examined viruses. Nucleotide diversity of 0.0029 per base (the average number of nucleotide substitutions of 3.3 per 1,131 base pairs) in the TK gene in the clinical isolates was comparable to 0.0037 per base of the whole HSV-1 genome in Japanese isolates reported previously. PCR-SSCP analysis of the acyclovir-resistant strains easily detected aberrantly shifted bands by comparing them with those of the parental strain, followed by the quick determination of mutated sequences. These results suggest that detection of nucleotide changes of the TK gene is useful for serial observation of persistent or recurrent HSV infection as observed in immunocompromised hosts, but that it is not useful for screening drug-resistant viruses from nonepidemic clinical isolates because of the comparable genetic polymorphisms in the TK gene as in the whole HSV-1 genome.
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PMID:Polymorphisms of thymidine kinase gene in herpes simplex virus type 1: analysis of clinical isolates from herpetic keratitis patients and laboratory strains. 974 72

Herpetic stromal keratitis (HSK) is a CD4+ T cell-controlled immunopathologic lesion in the eye that results from infection with herpes simplex virus (HSV). Target Ags involved in HSK remain undefined. In this study, we determined if HSK could be induced in animals genetically incapable of generating HSV Ag-specific CD4+ T cells. Mice bearing transgenic TCR specific to OVA peptide 323-339 (DO11.10) were crossed to SCID mice whose offspring (Tg-SCID) possessed CD4+ T cells, >98% of which expressed the OVA peptide-specific TCR. HSV infection of Tg-SCID mice was lethal, and mice failed to generate detectable T cell responses even after repeated immunization with a mutant avirulent virus (AN-1). Immunization with AN-1 virus followed by ocular challenge with HSV resulted in ocular inflammation before encephalitis, in contrast to the protection conferred in the control BALB/c and DO11.10 mice. These results indicate that clinical HSK may not require viral Ag recognition by CD4+ T cells and that T cells of irrelevant specificity can be recruited, activated, and driven into effector function in the HSV-infected cornea. This is suggested to represent a bystander activation effect resulting from the presence of proinflammatory mediators resulting from HSV replication.
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PMID:Virus-induced immunoinflammatory lesions in the absence of viral antigen recognition. 978 Feb 5

Cytokines are very important in the host defense system, and play a critical role in protection against bacterial and viral infections. Cytokines are also involved in the pathogenesis and development of symptoms in infections. In this article, Helicobacter pylori (H. pylori) infection as bacterial infection, and influenza virus infection, encephalomyocarditis virus (EMCV) infection, and herpes simplex virus (HSV) infection as viral infection are mentioned. In H. pylori infection, various chemokines, especially interleukin (IL)-8, induce inflammatory responses in the gastroduodenal mucosa. Furthermore, IL-6, IL-7, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma are involved in both protection and pathogenesis. In influenza virus infection, IFN-alpha/beta, IFN-gamma, and IL-6 play protective roles. In EMCV infection, IL-6 and TNF-alpha play important roles as a protective and exacerbative factor in acute myocarditis, respectively. Furthermore, in HSV infection, the production of inflammatory cytokines is closely correlated with the pathogenesis of herpetic keratitis, and IFN-gamma plays an important role in enhancing viral clearance from the cornea and trigeminal ganglions.
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PMID:Expression of cytokines in bacterial and viral infections and their biochemical aspects. 1073 41

An animal model has been developed to clarify the mechanism for spread of herpes simplex virus (HSV) from neuron to epithelial cells in herpetic epithelial keratitis. HSV was introduced into the murine trigeminal ganglion via stereotaxic guided injection. After 2 to 5 days, the animals were euthanized. Ganglia and corneas were prepared for light and electron microscopic immunocytochemistry with antisera to HSV. At 2 days, labeled axons were identified in the stromal layer. At 3 days, we could detect immunoreactive profiles of trigeminal ganglion cell axons that contained many vesicular structures. By 3 and 4 days, the infection had spread to all layers of epithelium, and the center of a region of infected epithelium appeared thinned. At 5 day, fewer basal cells appeared infected, although infection persisted in superficial cells where it had expanded laterally. Mature HSV was found in the extracellular space surrounding wing and squamous cells. Viral antigen was expressed in small pits along the apical surfaces of wing and squamous cells but not at the basal surface of these cells or on basal cells. This polarized expression of viral antigen resulted in the spread of HSV to superficial cells and limited lateral spread to neighboring basal cells. The pathogenesis of HSV infection in these mice may serve as a model of the human recurrent epithelial disease in the progression of focal sites of infection and transfer from basal to superficial cells.
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PMID:The spread of herpes simplex virus type 1 from trigeminal neurons to the murine cornea: an immunoelectron microscopy study. 1077 16

This report analyzes the role of vascular endothelial growth factor (VEGF)-induced angiogenesis in the immunoinflammatory lesion stromal keratitis induced by ocular infection with herpes simplex virus (HSV). Our results show that infection with replication-competent, but not mutant, viruses results in the expression of VEGF mRNA and protein in the cornea. This a rapid event, with VEGF mRNA detectable by 12 h postinfection (p.i.) and proteins detectable by 24 h p.i. VEGF production occurred both in the virus-infected corneal epithelium and in the underlying stroma, in which viral antigens were undetectable. In the stroma, VEGF was produced by inflammatory cells; these initially were predominantly polymorphonuclear leukocytes (PMN), but at later time points both PMN and macrophage-like cells were VEGF producers. In the epithelium, the major site of VEGF-expressing cells in early infection, the infected cells themselves were usually negative for VEGF. Similarly, in vitro infection studies indicated that the cells which produced VEGF were not those which expressed virus. Attesting to the possible role of VEGF-induced angiogenesis in the pathogenesis of herpetic stromal keratitis were experiments showing that VEGF inhibition with mFlt(1-3)-immunoglobulin G diminished angiogenesis and the severity of lesions after HSV infection. These observations are the first to evaluate VEGF-induced angiogenesis in the pathogenesis of stromal keratitis. Our results indicate that the control of angiogenesis represents a useful adjunct to therapy of herpetic ocular disease, an important cause of human blindness.
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PMID:Contribution of vascular endothelial growth factor in the neovascularization process during the pathogenesis of herpetic stromal keratitis. 1155 16


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