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 development of new antiviral agents has gained increasing momentum. It has kept pace with the identification of specific sites ("targets") in the virus replicative cycle at which potential antiviral drug can interact. The current armamentarium of available antiviral drugs consists of amantadine and rimantadine (against influenza A), ribavirin (against respiratory syncytial virus infection), idoxuridine and trifluridine (against herpetic keratitis), vidarabine and acyclovir (against herpes simplex virus infections), ganciclovir (against cytomegalovirus infections) and Retrovir (against AIDS). Various new compounds have been found which selectively inhibit those viruses [i.e. adenovirus, varicella-zoster virus, thymidine kinase-deficient (TK-) herpes simplex virus strains, and rhinoviruses] that are insensitive or poorly sensitive to the presently available antivirals. Several new compounds have also proven active against human immunodeficiency virus, the causative agent of AIDS; and, as a spin-off of the search for anti-AIDS drugs, new agents may also be expected that are effective against other retrovirus infections as well as hepadnavirus (i.e. hepatitis B virus) infections.
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PMID:New acquisitions in the chemotherapy of viral infections. 216 18

Interferons (IFN) are potent antiviral, cytostatic-cytotoxic and immunomodulatory agents. Although gene technology has made available an unlimited supply of all different kinds and types of IFN, their basic modes of action have not been clarified up to now. The therapeutic effects proven differ gradually between the individual disease entities. They comprise prophylaxis, prevention of recurrences and direct therapeutic effect, either of reducing the actual disease symptoms, or of inducing a complete recovery. For the following viral diseases a positive therapeutic effect has been shown: infections by herpes-viruses (herpes simplex keratitis , herpes zoster, herpes simplex), cytomegalovirus infections, chronic-hepatitis B virus infection, acute respiratory virus infections by rhino-, corona- and influenza viruses. Especially for the group of virus-associated tumors and papillomas, IFN is considered to be therapeutically effective. IFN has been accepted to be the first line treatment for laryngeal papillomatosis. In condylomata acuminata too, IFN is a potent therapeutic agent. Moreover, IFN represents the most effective therapeutic modality for Kaposi's sarcoma in patient with AIDS. Hairy cell leukemia, malignant lymphoma, multiple myeloma, melanoma and hypernephroma are the malignancies, for which a therapeutic effect of IFN could be proven. Furthermore, IFN is considered to be the therapy of first choice for hairy cell leukemias. Although there are some signs, that IFN could be a potent agent for adjuvant therapy, this question can not be answered - not even on principle - because of lacking sufficient data so far. Up to date, the therapeutic efficacy of IFN seems to be established only for hairy cell leukemia, laryngeal papillomatosis, Kaposi's sarcoma in patients with AIDS and partly for condylomata acuminata. For all other indications, first of all, sufficient phase-II-study data will have to be evaluated, before prospectively controlled studies, comparing the IFN treatment results with placebo and standard therapy results, can be initiated for the individual disease entities. Then, it will be possible to assess the therapeutic efficacy of IFN. Already now, IFN represent a valuable enrichment of the therapeutic modalities for malignancies and viral diseases.
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PMID:[Current status of interferon therapy]. 242 97

Stromal keratitis is typically the consequence of infection with herpes simplex virus type 1 (HSV-1). The pathogenesis of this disease remains elusive, although it is generally believed that there is an important immunological component. It has been proposed that stromal keratitis is mediated by virus-specific T lymphocytes of the delayed hypersensitivity type. However, while virtually all individuals infected with HSV-1 develop delayed hypersensitivity, only a small fraction actually develop stromal keratitis. To explain this discrepancy, we reasoned as follows: epidermal Langerhans cells are believed to be crucial to the induction of delayed hypersensitivity; since the cornea normally contains few or no cells of this type, the presence of Langerhans cells in the central corneal epithelium at the time of virus infection might promote the development of stromal keratitis. To test this hypothesis, cautery wounds of central regions of mouse corneas were used to induce migration of Langerhans cells into the corneal epithelium. These mice were then infected with HSV-1 on the ipsilateral snout, an infection that results in zosteriform spread of virus via the trigeminal nerve into the anterior segment of the ipsilateral eye within 3-5 days after inoculation. We found that the eyes of cauterized mice displayed a very high incidence of severe stromal keratitis. By contrast, non-cauterized corneas of control, snout-infected mice displayed much less evidence of stromal disease. Moreover, the rapidity of onset of systemic delayed hypersensitivity to HSV-1 was accelerated in the mice with cauterized corneas, compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunobiology of Langerhans cells on the ocular surface. II. Role of central corneal Langerhans cells in stromal keratitis following experimental HSV-1 infection in mice. 256 60

Acyclovir (aciclovir) is a nucleoside antiviral drug with antiviral activity in vitro against members of the herpes group of DNA viruses. As an established treatment of herpes simplex infection, intravenous, oral and to a lesser extent topical formulations of acyclovir provide significant therapeutic benefit in genital herpes simplex and recurrent orofacial herpes simplex. The effect of acyclovir therapy is maximised by early initiation of treatment, especially in non-primary infection which tends to have a less protracted course than the primary episode. Long term prophylactic oral acyclovir, in patients with frequent episodes of genital herpes simplex, totally suppresses recurrences in the majority of subjects; as with other infections responding to acyclovir, viral latency is not eradicated and pretreatment frequencies of recurrence return after discontinuation of treatment. Caution should accompany the prophylactic use of acyclovir in the general population, due to the theoretical risk of the emergence of viral strains resistant to acyclovir and other agents whose mechanism of action is dependent on viral thymidine kinase. Intravenous acyclovir is the treatment of choice in biopsy-proven herpes simplex encephalitis in adults, and has also been successful in the treatment of disseminated herpes simplex in pregnancy and herpes neonatorium. Intravenous and oral acyclovir protect against dissemination and progression of varicella zoster virus infection, but do not protect against post-herpetic neuralgia. In immunocompromised patients, intravenous, oral and topical acyclovir shorten the clinical course of herpes simplex infections while prophylaxis with oral or intravenous dosage forms suppresses reactivation of infection during the period of drug administration. Ophthalmic application of 3% acyclovir ointment rapidly heals herpetic dendritic corneal ulcers and superficial herpetic keratitis. Thus, despite an inability to eradicate latent virus, acyclovir administered in therapeutic or prophylactic fashion is now the standard antiviral therapy in several manifestations of herpes simplex virus infection, and indeed represents a major advance in this regard. With the exception of varicella zoster virus infections, early optimism concerning the use of the drug in diseases due to other herpes viruses has generally not been supported in clinical investigations.
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PMID:Acyclovir. An updated review of its antiviral activity, pharmacokinetic properties and therapeutic efficacy. 265 90

This review of ten years of experience presents the results of clinical use of human beta-interferon (Frone) in viral ocular disease. Two forms of human beta-interferon have been used: (a) Frone cream 20,000 IU/g (Inter-Yeda Ltd.) for local treatment and prevention of HSV-1 periocular skin lesions and for Herpes zoster ophthalmicus. (b) Frone eye drops (500,000-1,000,000 U) for prophylaxis and treatment of adenovirus infections and for prevention of recurrent HSV-1 keratitis. Our results show that Frone cream or drops, applied at an early stage, is: (a) Effective in significantly shortening the course of the disease; (b) Has a drying effect on herpetic skin lesions, and tear secretion in adeno viral disease; (c) Reduces the frequency from 1.2 to 0.04 attacks per year for patients with known biological rhythm of the disease; (d) Prevents subepithelial keratitis in 45% of the study population; (e) Prophylactic treatment of interferon in families reduces the incidence of contamination from 65% to 20%.
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PMID:Ten years of experience with human fibroblast interferon in treatment of viral ophthalmic infections. 307 9

Corneal complications of herpes zoster ophthalmicus include pseudodendritic keratitis, late mucous adherent keratopathy, varied forms of stromal keratitis, and exposure/neurotrophic keratopathy. Prophylactic therapy of acute herpes zoster ophthalmicus with oral acyclovir is of proven benefit in reducing the incidence of early pseudodendritic keratopathy and stromal keratitis but has no evident effect on exposure/neurotrophic keratopathy. Although early pseudodendritic keratitis is due to virus infection of epithelial cells, it is self-limited and does not require topical antiviral therapy. Stromal keratitis and associated epithelial mucous adherent keratopathy are responsive to topical corticosteroids but chronic therapy is often required and may prolong the duration of keratitis and result in cataract or secondary glaucoma. Exposure and neurotrophic keratopathy may respond to topical lubricants and correction of lid abnormalities but severely affected corneas may require tarsorrhaphy or conjunctival flap to maintain corneal integrity.
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PMID:Corneal complications of herpes zoster ophthalmicus. Prevention and treatment. 325 20

Of 94 patients with acute herpes zoster ophthalmicus who were seen during a six-year period, 61 had corneal involvement. The corneal complications in the order of chronological clinical occurrence were punctate epithelial keratitis in 51%, early pseudodendrites in 51%, anterior stromal infiltrates in 41%, sclerokeratitis in 1%, kerato-uveitis/endothelitis in 34%, serpiginous ulceration in 7%, delayed corneal mucous plaques in 13%, disciform keratitis in 10%, neurotrophic keratitis in 25%, and exposure keratitis in 11%. Some of the earlier lesions seemed to result from viral infection, whereas later lesions resulted from limbal vasculitis, an immunologic mechanism to soluble viral antigen, a delayed hypersensitivity reaction, or damage to nerves and tissues. An elucidation of the lesions awaits better viral and immunologic detection techniques and further histopathologic study. Modern topical and systemic antiviral therapy, corticosteroids, and surgery have a role in treatment.
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PMID:Corneal complications from herpes zoster ophthalmicus. 387 48

A 37-year-old man developed an acute follicular conjunctivitis with preauricular lymphadenopathy believed to be epidemic keratoconjunctivitis. On the eighth day of his disease, subepithelial dendritic opacities developed in the cornea which were not typical of either epidemic keratoconjunctivitis or herpetic keratitis. A diagnosis of primary herpes simplex virus infection was established by positive viral culture and a rise in serum antibody titer to herpes simplex virus. Subepithelial dendritic keratitis as a manifestation of herpes simplex infection of the cornea has not been previously described. The lesions seen in this patient were not reproducible in rabbits and we believe they represent an unusual host response to the virus. This form of herpetic keratoconjunctivitis is extremely difficult to differentiate from epidemic keratoconjunctivitis. Corticosteroids should be used with caution in cases that are not completely typical of epidemic keratoconjunctivitis.
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PMID:Primary herpes simplex subepithelial dendritic keratitis. 626 83

The clinical studies reviewed here indicated the usefulness of topical application of Human-fibroblast-derived (Beta) interferon (Hu1FN-B) in treatment of Adeno-8 Epidemic-keratoconjunctivitis. A week treatment with 2-5 x 10(5) reference units daily doses, starting early as possible, reduced the length of the disease from 22 day to a week, and almost totally prevented the appearance of subepithelial keratitis which occurred in 57% of the control group. Possibly interferon should be given also prophylactically to individuals exposed to contagion. Our results encourage further investigation on the Hu1 FN-B use as a drug for treatment and prevention of viral infection.
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PMID:Clinical effect of human-fibroblast-derived (Beta) interferon in treatment of adeno-virus epidemic keratoconjunctivitis and its complications. 630 37

Acute ocular infection followed both intracerebral and intranasal inoculation of herpes simplex type I virus (HSVI) in mice. Eye infections were a terminal complication of fatal encephalitis. After intracerebral inoculation HSVI spread directly along the optic nerves to infect the retina provoking a necrotizing retinitis. In contrast after intranasal inoculation, HSVI spread via the fifth cranial nerve to the anterior chamber of the eye producing keratitis and uveitis. Necrotizing retinitis was also produced by intracerebral inoculation of mice with a drug-resistant mutant HSVI known to have relatively low neurovirulence. These animals developed only mild encephalitis but this was associated with florid retinitis. The mice survived cerebral infection with the mutant virus and several weeks after initial inoculation cataracts were observed. There was no evidence, at any time, of virus infection of lens epithelium and cataracts appeared to be a non-specific consequence of retinal injury. It is suggested that these examples of murine ocular infection provide animal models for herpetic eye lesions in man and thus may elucidate the pathogenesis of herpetic keratitis, retinitis and cataract.
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PMID:An animal model of ocular herpes. Keratitis, retinitis and cataract in the mouse. 633 86


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