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)

Herpes simplex disciform keratitis is a difficult condition. The general feeling is that it is an immune disease, mediated by the virus, possibly located in the endothelial cells. It is frequently combined with inflammation in the trabecular meshwork and with uveitis. There is some controversy in relation to treatment and it has been suggested that anti-virals will control herpetic disciform keratitis, particularly if the patient has never had steroids previously. The authors of this paper have, in the past, published data which showed that Acyclovir, with corticosteroid, was necessary in the management of disciform keratitis. The data suggested that Acyclovir on its own was not effective. It remained to be answered whether Acyclovir on its own would be effective in patients who never had steroids for any reason previously. This paper demonstrates clearly that it is necessary, irrespective of whether patients have had steroids in the past or not, to combine corticosteroids with Acyclovir in the management of herpetic disciform keratitis. Acyclovir, on its own, is shown to be ineffective. It has also been suggested that Acyclovir is non-toxic. In a general way this is true, but the authors suggest that Acyclovir ointment does produce a punctate keratitis in patients with tear film disease, and that oral Acyclovir is preferable in such patients.
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PMID:The current management of herpetic eye disease. 142 35

HSV-1 multiplication rates have been shown to vary in different tissues and the rate of multiplication may correlate with susceptibility to antiviral chemotherapy. Herpetic stromal keratitis is a necrotizing condition refractive to antiviral therapy and this lack of antiviral efficacy in stromal disease may be the result of very low rates of viral replication in the corneal stromal keratocytes. In this study, we investigated the efficacy of antiviral drugs in an in vitro system in which the virus multiplication rate is slow. In this system, the reduced rate of virus multiplication is achieved by a reduction in the incubation temperature. Vero cells were infected at one of several multiplicities of infection with McKrae strain HSV-1 and incubated for 24, 48, or 72 h at 26 or 36.5 degrees C in the presence or absence of trifluridine (50 micrograms/ml) or acyclovir (20 micrograms/ml). Both drugs suppressed viral replication at 36.5 degrees C. However, under some specific sets of conditions, trifluridine was not effective in suppressing viral replication in cells incubated at 26 degrees C. At this temperature, viral replication and cell metabolism are slowed to a pace which may be similar to that which occurs in corneal stromal keratocytes in vivo. Acyclovir significantly reduced HSV-1 replication under all conditions at 26 degrees C, indicating that the antiviral activity of this compound is effective in cells whose metabolic rate is slow and in which viral replication is taking place slowly.
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PMID:The effect of HSV multiplication rate on antiviral drug efficacy in vitro. 185 50

Clinico-virologic investigations and the availability of the new antiviral drug Acyclovir have changed our therapeutic approach to deep herpetic diseases. Treatment of the symptoms alone with steroids should now be avoided. Basic treatment should consist of optimal dosages of Acyclovir. However, additional steroid therapy is still necessary. Significant progress in the treatment of dendritic keratitis is to be expected as soon as high-titer interferon preparations become commercially available. Treatment of dendritic keratitis with a combination of a modern antiviral drug and high-titer interferon will reduce the average time the corneal epithelium takes to heal from the present 6 days to 3 days. While considerable progress has been made in the treatment of herpes, no more than a step in the right direction has been taken with herpes zoster varicellosus virus, owing to its greater resistance to Acyclovir.
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PMID:[Therapy of herpetic diseases of the anterior eye segment]. 241 40

The antiherpes virus effects of 9-(1,3-dihydroxy-2-propoxymethyl) guanine (DHPG) were studied in cell culture and in experimental herpetic keratitis in rabbits. In plaque reduction assays in Vero cell, the 50% inhibitory concentration (IC50) of DHPG was shown to be 0.1 microgram/ml against HSV-1. Combination of DHPG and Cyclocytidine (CC), produced a synergistic activity against kos strains of HSV-1. Whereas the combination of DHPG and Acyclovir (ACV) or Tai-Ding-An (TDA) resulted in an additive interaction against HSV-1. Topical application of 0.1% or 0.05% DHPG eyedrop was initiated 48h after virus inoculation, significant efficacy was obtained in rabbits with herpetic epithelial keratitis. But 0.025 and 0.01% DHPG eyedrop showed no effect. 0.1% DHPG has been shown to be effective in the topical treatment of herpetic stromal keratitis in the rabbits.
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PMID:[Experimental studies of 9-(1, 3-dihydroxy-2-propoxymethyl)-guanine(DHPG) against herpes simplex virus]. 248 39

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

Although most herpetic ocular infections in adults are caused by herpesvirus hominis type 1, several cases of culture proved HSV-2 ocular infection in adults have been described, with more severe and prolonged disease. In a screening for new antiherpetic compounds, we investigated the efficacy in vivo of a new compound, nitroderivative of D-glucosaminhydrochloride (GN-11) in comparison with D-glucosaminhydrochloride (GN), Acyclovir (ACV) and placebo against herpetic keratitis of herpes simplex type 2 in 4 x 4 eyes from 4 x 4 rabbits, respectively. ACV and GN-11 showed similar results. The treatment with GN-11 retarded the appearance of herpetic lesions, which were small and diffuse in comparison with the placebo group. A total recovery was obtained on the 12th day of the treatment. In the ACV treated group, a minimal number of small lesions appeared, but the eyes recovered normality on the 7th day of treatment. The appearance of acute herpetic keratitis was prevented by GN-11. Placebo and GN treated groups showed similar evolution, with lost vision and neurological involvement on the 7th day of infection.
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PMID:Antiviral activity of a D-glucosamine derivative against herpetic ulcers (HSV type 2) in rabbit cornea. 277 39

Four nucleoside analogues--acyclovir [9-(2-hydroxyethoxymethyl)guanine], bromovinyldeoxyuridine [(E)-5-(2-bromovinyl)-2-deoxyuridine], vinylarauracil 5-vinyl-1-beta-D-arabinofuranosyluracil and bromovinylarauracil [(E)-5-(2-bromovinyl)-1-beta-D-arabinofuranosyluracil]--were compared in the therapy of acute keratitis induced in the rabbit cornea by inoculation of the KUPKA strain of herpes simplex virus type 1 (HSV-1). In comparison to placebo-treated animals, the drugs reduced the mean plaque counts in conjunctival swabs as follows: acyclovir to 0.16-1.73%, bromovinyldeoxyuridine to 0.02-0.25%, vinylarauracil to 0.55-5.96% and bromovinylarauracil to 0.12-3.39% of control values. Latency was established to a most limited extent in 1 or 2 out of 5 rabbits treated with vinylarauracil or bromovinylarauracil, respectively. One or 6 out of 84 or 98 explanted ganglion fragments (1.3 or 6%) were positive for HSV-1 as compared to 72 fragments out of 173 (43%) from placebo-treated rabbits. Acyclovir and bromovinyldeoxyuridine completely prevented latency.
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PMID:Efficacy of (E)-5-(2-bromovinyl)- and 5-vinyl-1-beta-D-arabinofuranosyluracil against acute herpes simplex virus keratitis and the establishment of latency: comparison with acyclovir and bromovinyldeoxyuridine. 289 82

Acyclovir, an oral antiviral agent that inhibits viral DNA replication, was used to treat 27 patients (16 males, 11 females) (mean age, 50 years) with vision-threatening herpes simplex virus (HSV) infections. Twenty patients had active stromal keratitis or keratouveitis, four had controlled nonnecrotizing stromal keratitis but could not taper topical medications, and four eczema patients with previous HSV infections had intraocular surgery (1 of these patients also is included in the 20 with active stromal keratitis). All 20 patients with active stromal keratitis or keratouveitis improved on acyclovir, all four patients using acyclovir postoperatively were disease-free while on the drug, but only two of the four patients using acyclovir to assist tapering topical medications were successful. There has been only one recurrence during a cumulative 194 months while on acyclovir. Thirteen patients have remained on acyclovir, and three who stopped acyclovir had prompt recurrences. Acyclovir seems to be a promising adjunct antiviral agent for the treatment of recalcitrant epithelial, stromal, or uveal disease secondary to HSV.
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PMID:Oral acyclovir in the management of herpes simplex ocular infections. 317 10

We treated 45 patients with virologically verified dendritic keratitis with a combination of interferon and acyclovir 3% or with placebo and acyclovir 3% in a double-masked study. One drop of human leukocyte interferon (30 X 10(6) IU/ml) or albumin-placebo was administered daily. Acyclovir ointment was applied five times daily. The mean healing time of the corneal ulcers in 24 patients treated with interferon and acyclovir was 3.9 days and the mean healing time in 21 patients treated with placebo and acyclovir was seven days. The difference was significant (P less than .001).
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PMID:Combination therapy for dendritic keratitis with human leukocyte interferon and acyclovir. 618 16

Acyclovir is a potent and selective antiviral agent. Unfortunately, drug-resistant (acyclovir-resistant) mutants have already been reported in herpes simplex virus type 1 (HSV-1) orofacial infections. We have developed a laboratory acyclovir-resistant HSV-1 mutant. The natural course of acyclovir-resistant HSV-1 keratitis was found to be less virulent than that observed in wild type HSV-1 keratitis, but the rate of ganglionic latency was as high as that induced by the parental strain. In vitro studies and in vivo observation of rabbit corneas infected with acyclovir-resistant HSV-1 both demonstrated a significant sensitivity to vidarabine and bromovinyldeoxyuridine ([E]-5-[2-bromovinyl]-2'-deoxyuridine). The thymidine kinase activity of the acyclovir-resistant mutant was 69% of that of the wild type HSV-1.
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PMID:Herpes simplex acyclovir-resistant mutant in experimental keratouveitis. 631 52


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