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      Management of herpes simplex virus epithelial keratitis :

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          Herpes simplex epithelial and stromal keratitis: an epidemiologic update.

          Herpes simplex virus (HSV) is associated with a variety of ocular diseases, including epithelial and stromal keratitis. HSV can cause stromal opacification and is believed to be the leading cause of infectious blindness in the developed world. An improved understanding of the global burden of HSV keratitis, including the incidence of severe vision loss, could have a significant effect on prevention and treatment and place it in perspective among causes of corneal ulceration. We found that the global incidence of HSV keratitis is roughly 1.5 million, including 40,000 new cases of severe monocular visual impairment or blindness each year. We also discuss relevant epidemiologic issues regarding HSV epithelial and stromal disease. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Herpes simplex keratitis.

            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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              Is Open Access

              New strategies against drug resistance to herpes simplex virus

              Herpes simplex virus (HSV), a member of the Herpesviridae family, is a significant human pathogen that results in mucocutaneous lesions in the oral cavity or genital infections. Acyclovir (ACV) and related nucleoside analogues can successfully treat HSV infections, but the emergence of drug resistance to ACV has created a barrier for the treatment of HSV infections, especially in immunocompromised patients. There is an urgent need to explore new and effective tactics to circumvent drug resistance to HSV. This review summarises the current strategies in the development of new targets (the DNA helicase/primase (H/P) complex), new types of molecules (nature products) and new antiviral mechanisms (lethal mutagenesis of Janus-type nucleosides) to fight the drug resistance of HSV.
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                Author and article information

                Journal
                Current Opinion in Ophthalmology
                Current Opinion in Ophthalmology
                Ovid Technologies (Wolters Kluwer Health)
                1040-8738
                2018
                July 2018
                : 29
                : 4
                : 360-364
                Article
                10.1097/ICU.0000000000000483
                cb1bd243-d07e-4078-b18d-b142ef061f11
                © 2018
                History

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