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 indications for keratoplasty in treating herpes keratitis are currently declining because of recent progress in diagnosis and treatment. Clinically, corneal signs may be caused by HSV reactivation or a secondary anti-HSV immune response. Corneal opacification may be acute or the expression of sequela (meta-herpetic keratitis). The virus can be detected on a corneal surface sample by direct examination or cell culture, the only way to detect an infective virus. The detection of local antibody production in the aqueous humor is an inexpensive method, indicating the local immune anti-HSV response. Detection of HSV DNA using PCR is more sensitive, but the presence of HSV DNA within corneal tIssue may be more delicate to interpret. It is now proven that HSV can be transmitted through a corneal graft from donor to recipient, but no diagnostic test currently detects potentially infective corneas in eyebanks.
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PMID:[Clinical and diagnostic developments in corneal herpes]. 1517 11

Herpetic keratitis is characterized by spontaneous recurrences and a risk of vision loss, the latter being more serious when relapses are frequent and severe. Two clinical forms are commonly distinguished: epithelial keratitis, usually quickly resolved with topical antivirals, and stromal keratitis, which has a slower progression, even when both steroids and antivirals are used. Great strides have been made during the last 20 Years in the therapy of herpes keratitis, which is now considered and treated as a chronic disease. Randomized controlled studies definitively showed the decrease in spontaneous herpetic ocular events in patients treated with long-term oral acyclovir. The effectiveness of preventive treatment has also been shown during high-risk periods, especially ocular surgery, in patients with a history of herpes keratitis. However, the optimal duration and dosage of antiviral prevention have yet to be defined. We can also hope that in the future novel antiviral strategies such as vaccination will reduce the place of herpes keratitis as an indication for corneal graft.
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PMID:[The latest in herpes simplex keratitis therapy]. 1517 14

Herpes simplex virus infection of the eye is the leading cause of blindness due to infection in the US despite the availability of several antiviral drugs. Studies with animal models have shown that three factors, innate host resistance, the host adaptive immune response, and the strain of virus interact to determine whether an infection is asymptomatic or proceeds to the development of blinding keratitis (HSK). Of these, the role of adaptive immunity has received the most attention. This work has clearly shown that stromal keratitis is an immunopathological disease, most likely due to the induction of a delayed type hypersensitivity response. Substantially less is known about the role of specific host genes in resistance to HSK. The fact that different strains of virus display different disease phenotypes indicates that viral 'virulence' genes are critical. Of the 80 plus HSV genes, few have been formally tested for their role in HSV keratitis. Most studies of virulence genes to date have focused on a single gene or protein and large changes in disease phenotypes are usually measured. Large changes in the ability to cause disease are likely to reduce the fitness of the virus, thus such studies, although useful, do not mimic the natural situation. Viral gene products are known to interact with each other, and with host proteins and these interactions are critical in determining the outcome of infection. In reality, the 'constellation' of genes encoded by each particular strain is critical, and how this constellation of genes works together and with host proteins determines the outcome of an infection. The goal of this review is to discuss the current state of knowledge regarding the role of host and viral genes in HSV keratitis. The roles of specific genes that have been shown to influence keratitis are discussed. Recent data showing that different viral genes cooperate to influence disease severity and confirming that the constellation of genes within a particular strain determines the disease phenotype are also discussed, as are the methods used to test the role of viral genes in virulence. It will become apparent that there is a paucity of information regarding the function of many viral genes in keratitis. Improving our knowledge of the role of viral genes is critical for devising more effective treatments for this disease.
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PMID:The role of viral and host genes in corneal infection with herpes simplex virus type 1. 1586 67

The cornea is naturally transparent. Anything that interferes with the cornea's stromal architecture, contributes to blood vessel migration, increases corneal pigmentation, or predisposes to corneal edema, disrupts the corneas transparency and indicates corneal disease. The color, location, and shape and pattern of a corneal lesion can help in determining the underlying cause for the disease. Corneal disease is typically divided into congenital or acquired disorders. Congenital disorders, such as corneal dermoids are rare in cats, whereas acquired corneal disease associated with nonulcerative or ulcerative keratitis is common. Primary ocular disease, such as tear film instability, adenexal disease (medial canthal entropion, lagophthalmus, eyelid agenesis), and herpes keratitis are associated with the majority of acquired corneal disease in cats. Proliferative/eosinophilic keratitis, acute bullous keratopathy, and Florida keratopathy are common feline nonulcerative disorders. Nonprogressive ulcerative disease in cats, such as chronic corneal epithelial defects and corneal sequestration are more common than progressive corneal ulcerations.
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PMID:Feline corneal disease. 1594 22

Herpes stromal keratitis is an immunopathologic disease in the corneal stroma leading to scarring, opacity, and blindness, and it is an important problem in common corneal surgeries. Paradoxically, virus antigens are largely focused in the epithelial layer of the cornea and not in the stromal layer, and viral antigens are eliminated before stromal inflammation develops. It is not clear what drives inflammation, whether viral antigens are necessary, or how viral antigens reach the stroma. It has been proposed that herpes simplex virus (HSV) travels from the corneal epithelium to sensory ganglia then returns to the stroma to cause disease. However, there is also evidence of HSV DNA and infectious virus persistent in corneas, and HSV can be transmitted to transplant recipients. To determine whether HSV resident in the cornea could cause herpes stromal keratitis, we constructed an HSV US9- mutant that had diminished capacity to move in neuronal axons. US9- HSV replicated and spread normally in the mouse corneal epithelium and to the trigeminal ganglia. However, US9- HSV was unable to return from ganglia to the cornea and failed to cause periocular skin disease, which requires zosteriform spread from neurons. Nevertheless, US9- HSV caused keratitis. Therefore, herpes keratitis can occur without anterograde transport from ganglia to the cornea, probably mediated by virus persistent in the cornea.
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PMID:Herpes keratitis in the absence of anterograde transport of virus from sensory ganglia to the cornea. 1605 58

In primary ocular herpes simplex virus (HSV) infection, nitric oxide may function to control viral replication and herpetic stromal keratitis (HSK) lesions. Recurrent HSK, manifested as corneal opacity and neovascularization, is the potentially blinding sequel to primary infection. Here, we assess the effects of nitric oxide synthase inhibition on a mouse model of recurrent HSK. In preliminary primary infection experiments, NIH inbred mice treated with aminoguanidine, an inhibitor of inducible nitric oxide synthase (iNOS), experienced no changes in post-infection tear, brain, or ganglia virus titers, but encephalitis-related mortality was elevated. After UV-B stimulated viral reactivation, iNOS inhibition did not affect virus shedding or clinical disease. In contrast to primary HSK, there was no exacerbation of mortality in recurrent disease. Our findings indicate that nitric oxide can be neuroprotective without antiviral effects in primary HSK, and does not play a significant role in the pathogenesis of recurrent HSK. Compared with data from other mouse strains, this work suggests that there may be a genetic component to the importance of NO in controlling ocular HSV infection.
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PMID:The effects of aminoguanidine on primary and recurrent ocular herpes simplex virus infection. 1612 22

A 76-year-old man presented with features of bilateral herpes simplex virus (HSV) keratitis. It was found to be recurrence of bilateral HSV keratitis following the use of Bimatoprost eye drops for uncontrolled intraocular pressure in a case of bilateral primary open-angle glaucoma.
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PMID:Recurrence of bilateral herpes simplex virus keratitis following bimatoprost use. 1653 73

Herpes simplex keratitis (HSK) results from an infection with the herpes simplex virus type 1 (HSV-1) also known as human herpesvirus type 1 (HHV-1). Primary infection may involve an ocular or non-ocular site, following which latency might be established principally in the trigeminal ganglion but also in the cornea. During latency, the virus appears as a circular episome associated with histones with active transcription only from the region encoding the latency-associated transcript (LAT). The LAT region is implicated in neuronal survival, anti-apoptosis, virulence, suppression of transcription, establishment of and reactivation from latency. The initial keratitis may develop after infection through the "front door route" (entry into the ocular surface from droplet spread) or "back door route" (spread to the eye from a non-ocular site, principally the mouth). The initial ocular infection may be mild. Visual morbidity results from recurrent keratitis, which leads to corneal scarring, thinning and neovascularisation. Although, recurrent disease may potentially occur through anterograde axonal spread from the trigeminal ganglion to the cornea, recent evidence suggests that HSV-1 in the cornea may be another source of recurrent disease. The pathogenesis and severity of HSK is largely determined by an interaction between viral genes encoded by the strain of HSV-1 and the make up of the host's immune system. Herpetic stromal disease is due to the immune response to virus within the cornea and the ability of the strain to cause corneal stromal disease is correlated with its ability to induce corneal vascularisation. The pathogenesis of corneal scarring and vascularisation is uncertain but appears to be a complex interaction of various cytokines, chemokines and growth factors either brought in by inflammatory cells or produced locally in response to HSV-1 infection. Evidence now suggests that HSV-1 infection disrupts the normal equilibrium between angiogenic and anti-angiogenic stimuli leading to vascularisation. Thrombospondin 1 and 2, matricellular proteins, involved in wound healing are potent anti-angiogenic factors and appear to be one of the key players. Elucidating their roles in corneal scarring and vascularisation may lead to improved therapies for HSK.
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PMID:Herpes simplex keratitis. 1680 55

Recently, a number of medications approved for nondermatologic use have proved useful against dermatologic diseases. This article reviews the dermatologic uses and effects of deferasirox, bortezomib, dasatinib, and cyclosporine eye drops. Deferasirox--an oral iron chelator--could be an effective treatment against porphyria cutanea tarda, hemochromatosis, and pathogens such as mucor that thrive in iron rich environments. Bortezomib, a proteasome inhibitor and multiple myeloma treatment, may be effective against nodular amyloid and has been effectively used against squamous cell carcinoma; although trials demonstrate it is ineffective against metastatic melanoma. Bortezomib has many cutaneous side effects including erythematous plaques or nodules, a generalized morbilliform erythema with ulcerations and fever, purpuric eruptions, leukocytoclastic vasculitis, Sweet's syndrome, and folliculitis. Dasatinib is a multi-targeted tyrosine kinase inhibitor active in vitro against most cell lines containing BCR-ABL mutations that confer resistance to imatinib. Dasatinib is likely to be effective against dermatofibroma sarcoma protuberans and cutaneous acute lymphoblastic leukemia, and has caused panniculitis. Cyclosporine 0.05% ocular emulsion (eye drops) are approved to treat dry eyes including dry eyes caused by collagen vascular disease. Cyclosporine eye drops might also have utility in treating eye pathology of ocular rosacea, atopic keratoconjunctivitis, graft versus host disease, herpes keratitis, chronic sarcoidosis of the conjunctiva, conjunctival manifestations of actinic prurigo, keratitis of keratitis-ichthyosis deafness (KID) syndrome, and lichen planus-related kerato-conjunctivitis. This article speculates that cyclosporine eye drops would also be useful for any disease causing ectropion or eclabion of the eye as well as toxic epidermal necrolysis-related eye pathology (in particular corneal scarring).
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PMID:A review of deferasirox, bortezomib, dasatinib, and cyclosporine eye drops: possible uses and known side effects in cutaneous medicine. 1737 1

Herpes simplex virus (HSV) keratitis is a common cause of ocular and visual morbidity. In this article, we systematically review published randomized clinical trials (RCTs) for HSV epithelial and stromal keratitis in order to establish a rational evidence-based foundation for treatment of these disorders. Articles for review were identified in the MEDLINE database from January 1, 1966, to May 30, 2006. Our review criteria stipulated that each study be performed in prospective, randomized, and double-blinded fashion, that it be controlled, and that it rely on specific clinical criteria for diagnosis and outcome. Of articles thus identified in the English language press, 38 articles met our review criteria, 30 for HSV epithelial keratitis and 8 (comprising 7 RCTs) for HSV stromal keratitis. From these studies, we concluded that the best evidence from treatment trials on HSV epithelial keratitis supports the use of topical trifluridine and topical or oral acyclovir, and suggests a possible additional benefit for topical interferon. The best evidence from RCTs for HSV stromal keratitis supports the use of topical corticosteroids given together with a prophylactic antiviral to shorten the duration of active HSV stromal keratitis, and the use of long-term suppressive oral acyclovir therapy to reduce the incidence of recurrent HSV keratitis.
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PMID:Evidence-based treatment of herpes simplex virus keratitis: a systematic review. 1766 Aug 97


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