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)

Likopide (N-acetylglucosamine-(beta 1-4)-N-acetylmuramyl-alanyl-D-isoglutamine) is a synthetic analog of muramylpeptides, characterized by immunomodulating properties and increasing the nonspecific resistance to infections. Seventy patients with ophthalmic herpes were examined, 35 of these were treated with likopide and 35 were administered placebo. Fifty-two of these suffered from stromal keratitis with ulceration and 18 had no ulcers. The trials were carried out by the double blind test with placebo. Likopide was administered orally in 10 mg tablets twice daily according to the following protocol: 3 days of treatment, 3-day interval, and 3-day treatment. All the patients were administered local specific (acyclovir ointment) and general symptomatic therapy. Immunological studies were carried out before and after therapy. Clinical assessment showed a reliably high therapeutic efficacy of likopide, its total value (excellent and good results) being as high as 88.5%. The mean duration of therapy with likopide was 11.4 +/- 0.4 days versus 15.2 +/- 0.9 days in the placebo group. Judging by the recovery criteria (arrest of inflammation, epithelization of the cornea, resorption of corneal infiltration and edema, resorption of iritis) likopide reliably accelerated healing and ensured a higher increase of vision acuity. Likopide reliably decreased the rate of detection of herpes simplex virus antigen in the involved eye conjunctiva in comparison with the placebo group patients (97.1% of negative cases versus 60%). The drug was well tolerated by the patients, no side effects were observed. Skin allergic tests with likopide showed no drug allergies.
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PMID:[Therapy of stromal herpetic keratitis with a new immunomodulator likopide]. 938 37

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

Viral infection is sometimes associated with the initiation or exacerbation of autoimmune disease, although the underlying mechanisms remain unclear. One proposed mechanism is that viral determinants that mimic host antigens trigger self-reactive T cell clones to destroy host tissue. An epitope expressed by a coat protein of herpes simplex virus-type 1 (HSV-1) KOS strain has now been shown to be recognized by autoreactive T cells that target corneal antigens in a murine model of autoimmune herpes stromal keratitis. Mutant HSV-1 viruses that lacked this epitope did not induce autoimmune disease. Thus, expression of molecular mimics can influence the development of autoimmune disease after viral infection.
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PMID:Molecular mimicry by herpes simplex virus-type 1: autoimmune disease after viral infection. 950 4

In patients with herpes virus dendritic epithelial keratitis, the pathologic morphogenesis of the dendritic lesion was investigated by means of impression cytology. Impression specimens were taken from the lesions of 24 consecutive patients assessed with a slit lamp biomicroscope. After a Millipore membrane impression was stained with hematoxylin-eosin and examined by light microscope, cellular patterns were analyzed. The results of these examinations showed that most cells were epithelial cells; there were also occasional multinucleated syncytial giant cells, inclusion bodies and inflammatory cells. Basal epithelial cells were most prominent at the actively infected lesion, whereas superficial epithelial cells were shown at the margin of the active lesion and terminal bulb. These findings suggest that in dendritic keratitis, viral spread and replication in the dendritic keratitis may progress through basal epithelial cells along the nerve within the basal epithelium-stromal interface.
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PMID:Infectivity of basal epithelial cells in herpetic dendritic epithelial keratitis. 951 Jun 49

Herpes simplex virus type 1 (HSV-1) infection of the murine cornea results in a tissue-destructive inflammatory response. In this study we show that virus infection induces the synthesis of macrophage inflammatory protein-2 (MIP-2), MIP-1alpha, and monocyte chemoattractant protein-1 (MCP-1). However, only the production of MIP-2 and MIP-1alpha coincided with the influx of leukocytes into the cornea. IL-10 treatment markedly suppressed chemokine message and protein synthesis in vivo. Local administration of IL-10 also dramatically reduced the number of T cells and neutrophils migrating into the cornea and suppressed the severity of corneal disease. The inflammatory response could also be suppressed by the passive transfer of neutralizing antibody to MIP-1alpha but not MCP-1. We conclude that local IL-10 administration can suppress chemokine synthesis, thereby ameliorating corneal disease. Furthermore, our results indicate that MIP-1alpha plays a major role in herpes stromal keratitis development, whereas MCP-1 does not.
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PMID:Chemokine synthesis in the HSV-1-infected cornea and its suppression by interleukin-10. 954 79

The requirement for T cell costimulation at sites of infection and inflammation is unresolved. Herpes stromal keratitis (HSK) is a CD4+ T cell-regulated inflammatory response to herpes simplex virus type 1 infection of the cornea. Our findings suggest that susceptibility to HSK is determined by the microenvironment of the infected cornea. The cornea is normally devoid of Langerhans cells (LC), but these APC are present in the surrounding conjunctiva, and migrate into the cornea following infection. The costimulatory molecule B7-2 was constitutively expressed on LC in conjunctiva, but B7-1 was not detectable until 3 days postinfection. LC were the only cells in the cornea that expressed B7-1 through 7 days postinfection. B7-1 was expressed on some, but not all, migrating LC, suggesting that LC migration and B7-1 expression can be independently regulated. The early LC migration and B7-1 expression was independent of T cells, but T cells were required for the massive accumulation of B7-1+ LC in the cornea at the onset of inflammation. Local inhibition of B7-1 function within the infected cornea prevented HSK. Locally blocking B7-2 function did not reduce HSK incidence, but markedly reduce HSK severity. This is the first direct demonstration that naturally expressed B7 is required within an inflammatory site.
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PMID:B7 costimulatory requirements of T cells at an inflammatory site. 959 Feb 54

In the tissues of the herpes-infected eye of a rabbit the content of adenosine triphosphoric acid (ATP), glucose and pyroracemic acid decreases and the level of lactic acid rises, i.e. anaerobic glycolysis prevails over the aerobic decomposition of glucose. A sharp decrease in the amount of ATP in the cornea and the iris in herpetic keratitis is due to the increased consumption of ATP for the synthesis of DNA and polypeptides of herpes simplex virus, as well as to disturbances in the oxidation transformations of glucose linked with the increased proportion of anaerobic glycolysis.
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PMID:[Glycolytic metabolites and adenosine triphosphoric acid in the herpes-infected eye]. 966 12

Most conjunctival nevi are found during the two first decades of life. Beyond this period, the diagnosis must be assessed by histopathology. We report the case of a conjunctival nevus recently discovered in a 33-year-old patient who, additionally, was previously treated for herpetic disciform keratitis. The corneal scar decreased vision. A corneal graft and nevus excision were performed simultaneously. Histopathologic study confirmed the diagnosis of nevus and disclosed the corneal scar changes induced by herpes.
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PMID:[Association of nevus and herpetic keratitis sequela. Apropos of an anatomo-clinical case]. 1022 Dec 4

In reviewing the clinical features, diagnostic evaluations and therapies of the most common ocular viral infections we attempt to whet your appetite for attacking the numerous challenges in diagnosis and treatment of viral eye disease. The herpes viruses, HSV, VZV and CMV are the cause of significant ocular morbidity. HSV most commonly affects the cornea producing keratitis that can be recurrent and may lead to corneal clouding and neovascularisation. Manifestations can be purely infectious or immunological and treatment options must be tailored to the underlying pathophysiology. Herpes zoster ophthalmicus, caused by VZV infection of the first branch of the trigeminal nerve, produces a characteristic rash and can progress to keratitis and uveitis. HSV and VZV can cause retinitis in both immunocompetent and immunocompromised individuals. There has been a significant increase in the incidence of CMV retinitis since the beginning of the AIDS epidemic. We review the numerous new treatments, diagnostic tests and treatment strategies which have been developed in response to this potentially blinding retinal infection. Adenovirus produces an epidemic conjunctivitis and epidemic keratoconjunctivitis which are severe and extremely contagious conjunctival infections. HIV, molluscum contagiosum, EBV and rubeola also cause ocular diseases which are described.Copyright 1998 John Wiley & Sons, Ltd.
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PMID:Virus infections of the eye. 1039 8

Herpetic eye disease is common and is frequently associated with intraocular inflammation or uveitis. Despite recent advances in measuring anti-herpes virus antibodies and viral DNA in ocular fluids, diagnosis remains largely clinical. The two more common syndromes include anterior uveitis, often associated with keratitis, and the acute retinal necrosis (ARN) syndrome. Treatment is complex and requires careful monitoring to provide the appropriate balance of antiviral medication and corticosteroids. Long-term prophylaxis with oral antiviral agents may be required in selected patients to help prevent the vision-compromising complications associated with recurrences.
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PMID:Advances in diagnosis and management of herpetic uveitis. 1079 Dec 59


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