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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Herpes simplex virus infections are epidemic throughout developed countries, and recurrent herpes simplex keratitis is the most common cause of corneal blindness in these countries, NIH (1973). No available antiviral agent is capable of eradicating the state of viral ganglionic latency, and hence no effective treatment currently exists for prevention of viral re-activation from latency, with resultant recurrent infectious viral clinical manifestations. Putative triggers of re-activation include stress, sunburn, menses, trauma, and fever. These 'triggers' seem to share at least one common characteristic: the potential ability to influence intracellular cyclic nucleotide levels through the action of such first order messengers as catacolamines (stress, trauma) and/or arachadonic acid metabolites (sunburn, fever, trauma, and menses). We exploited an in vitro model of HSV ganglionic latency, and developed a model of in vitro organ culture ganglionic viral reactivation from latency. We then examined the effect of a variety of agents on this model. We found that agents which have been shown to elevate cyclic AMP levels consistently produce increased viral shedding (compared to control, spontaneous reactivation rate) in our model of viral reactivation from latency. In contrast, agents which have been shown to depress c-AMP levels and/or to elevate c-GMP levels inhibit viral reactivation from latency in this in vitro model. We conclude that intracellular cyclic nucleotide levels may influence events which control herpes simplex genome transcription.
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PMID:Evidence for the potential influence of cyclic nucleotides on maintenance of or reactivation from latency of herpes simplex virus in trigeminal ganglionic neurons. 255 43

Hematoporphyrin (HP), at concentrations as low as 0.5 microgram/ml, was found to inhibit the in vitro replication of influenza A and herpes simplex viruses, but not of several other viruses. The effect required exposure of the viruses or cells to visible light and was demonstrable when HP was administered shortly before virus inoculation or during the infection. In studies on the mechanism of action of HP, we found that in the presence of light, HP caused decomposition of GMP but not of various other nucleosides. It caused breakdown of yeast tRNA and inhibited polymerization of RNA and DNA by influenza virus and HSV-1-specific polymerases as well as some other polymerases isolated from bacterial and mammalian sources. Protective effects of HP and light were demonstrable in embryonated eggs infected with the WSN and PR8 strains of influenza A virus and in mice infected with the WSN strain. HSV-1-induced keratitis in rabbits and HSV-2-induced dermatitis in mice were not responsive to HP treatment.
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PMID:Photodynamic inactivation of influenza and herpes viruses by hematoporphyrin. 302 46