Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical features and the molecular epidemiology of primary herpes simplex virus type 1 (HSV-1) infection among children younger than 3 years of age were investigated in day-care nursery. Serial sera were assayed for anti-HSV-1 glycoprotein B antibody by enzyme-linked immunosorbent assay. Serologic examinations revealed 55 cases of primary HSV infection during the observation period. Fifty-one of them (93%) had typical herpetic gingivostomatitis, showing a high rate of clinically overt infection. Four outbreaks of herpetic gingivostomatitis were observed during the observation period. Forty-one children were infected with HSV-1 in the outbreaks. The rates of infection in the susceptible children were 81%, 73%, 78%, and 100%, respectively, in the four outbreaks. Restriction endonuclease analysis of DNA of isolated HSV revealed that only one strain of HSV-1 had been transmitted among children for a long period.
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PMID:Clinical manifestations of primary herpes simplex virus type 1 infection in a closed community. 184 35

A series of acute herpetic infections occurred among nurses and patients in a pediatric intensive care unit (PICU). Epidemiologic study revealed two separate time clusters of infections, one in early summer and another six weeks later. Restriction endonuclease analysis of DNA extracted from virus isolates showed that each time cluster was associated with a different genetic strain of herpes simplex virus (HSV) type 1 and provided evidence of cross infection between patients and nurses. Three nurses had herpetic whitlow; the husband of one had acute gingivostomatitis; a fourth nurse had acute pharyngitis. They had no previous history of HSV infection and sequential antibody testing of affected nurses showed 19S antibody in all initially positive serums, confirming primary infection. The data provide clear evidence that PICU personnel risk acquiring serious herpetic infections from patients and vice versa unless specific precautions are taken. Restriction endonuclease analysis of HSV DNA was useful in the epidemiologic study of the infections.
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PMID:Nosocomial herpetic infections in a pediatric intensive care unit. 625 25

A simple and practical method for typing and strain differentiation of herpes simplex virus (HSV) isolates, based upon analysis of the restriction endonuclease cleavage patterns of viral DNAs, was established by using unlabeled infected cell DNAs. The preparation of infected cell DNA is technically easier than that of purified viral DNA or of radiolabeled viral DNA. The method provides a powerful and practical tool for epidemiological and clinical studies of HSV infection, which can be performed in most diagnostic laboratories. In order to select suitable restriction endonucleases for the study of HSV isolates, the cleavage patterns of viral DNAs (strains MacIntyre, HF, UW-268, and SAV) with 12 enzymes were analyzed. Several enzymes, Bam HI, Kpn I, Pst I, Sal I, Sst I, and Xho I, were found to be useful for both typing and strain differentiation. With this method, HSV isolates from different individuals and from the same individual were analyzed by digestion of their infected cell DNAs with Bam HI. Six isolates from epidemiologically unrelated individuals were readily typed and differentiated from each other. Three isolates from the same individual showed very similar patterns. However, there was a small degree of difference between the first two isolates and the third isolate.
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PMID:A simple and practical method for typing and strain differentiation of herpes simplex virus using infected cell DNAs. 630 53

Three cases of neonatal disseminated herpes simplex virus (HSV) infection are reported. They were all due to different strains of HSV-1, according to restriction endonuclease studies, and they represent the first cluster of neonatal-HSV infection at Magee-Womens Hospital. The neonatal symptoms occurred early, suggesting intrauterine infection. None of the babies had mucocutaneous lesions, and the mothers were asymptomatic and had no history of previous genital HSV infection.
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PMID:A cluster of neonatal herpes simplex infections without mucocutaneous manifestations. 632 84

The 2',5'-oligoadenylate (2-5A) synthetase pathway, induced by interferon-alpha (IFN-alpha), has been shown to be responsible for the antiviral action of IFN-alpha against some viruses. Studies were done to determine the role of this pathway in the anti-herpes simplex virus (HSV) action of IFN-alpha alone or in combination with acyclovir (ACV), a combination that leads to synergistic anti-HSV activity. Treatment of human corneal cells or Vero cells with 100 IU/ml of IFN-alpha induced expression of 2-5A synthetase mRNA and a 10-fold increase in 2-5A synthetase production compared with untreated cells. HSV infection alone did not induce 2-5A synthetase production, but when IFN-alpha-treated cells were infected with HSV, enzyme level was significantly increased (p < 0.05) compared with that in IFN-alpha-treated, uninfected cells. HSV infection actually decreased the level of 2-5A synthetase mRNA in IFN-alpha-treated cells. Although IFN-alpha treatment induced high levels of 2-5A synthetase with or without HSV infection, no activation of the latent endonuclease was detected by specific cleavage of ribosomal RNA. Treatment of infected cells with 5 microM ACV alone or combined with IFN-alpha did not increase 2-5A synthetase or endonuclease activities above those detected in cells not treated with ACV. The data indicate that the 2-5A synthetase pathway was inducible in corneal cells and Vero cells but did not appear to contribute to the anti-HSV activity of IFN-alpha alone or the synergistic activity of IFN-alpha combined with ACV.
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PMID:2',5'-oligoadenylate synthetase in interferon-alpha- and acyclovir-treated herpes simplex virus-infected cells. 764 30

The herpes simplex virus (HSV) virion host shutoff (Vhs) protein is an endoribonuclease that accelerates decay of many host and viral mRNAs. Purified Vhs does not distinguish mRNAs from nonmessenger RNAs and cuts target RNAs at many sites, yet within infected cells it is targeted to mRNAs and cleaves those mRNAs at preferred sites including, for some, regions of translation initiation. This targeting may result in part from Vhs binding to the translation initiation factor eIF4H; in particular, several mutations in Vhs that abrogate its binding to eIF4H also abolish its mRNA-degradative activity, even though the mutant proteins retain endonuclease activity. To further investigate the role of eIF4H in Vhs activity, HeLa cells were depleted of eIF4H or other proteins by transfection with small interfering RNAs (siRNAs) 48 h prior to infection or mock infection in the presence of actinomycin D. Cellular mRNA levels were then assayed 5 h after infection. In cells transfected with an siRNA for the housekeeping enzyme glyceraldehyde-3-phosphate dehydrogenase, wild-type HSV infection reduced beta-actin mRNA levels to between 20 and 30% of those in mock-infected cells, indicative of a normal Vhs activity. In contrast, in cells transfected with any of three eIF4H siRNAs, beta-actin mRNA levels were indistinguishable in infected and mock-infected cells, suggesting that eIF4H depletion impeded Vhs-mediated degradation. Depletion of the related factor eIF4B did not affect Vhs activity. The data suggest that eIF4H binding is required for Vhs-induced degradation of many mRNAs, perhaps by targeting Vhs to mRNAs and to preferred sites within mRNAs.
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PMID:Small interfering RNAs that deplete the cellular translation factor eIF4H impede mRNA degradation by the virion host shutoff protein of herpes simplex virus. 1844 41

A large portion of the global population carries latent herpes simplex virus (HSV), which can periodically reactivate, resulting in asymptomatic shedding or formation of ulcerative lesions. Current anti-HSV drugs do not eliminate latent virus from sensory neurons where HSV resides, and therefore do not eliminate the risk of transmission or recurrent disease. Here, we report the ability of HSV-specific endonucleases to induce mutations of essential HSV genes both in cultured neurons and in latently infected mice. In neurons, viral genomes are susceptible to endonuclease-mediated mutagenesis, regardless of the time of treatment after HSV infection, suggesting that both HSV lytic and latent forms can be targeted. Mutagenesis frequency after endonuclease exposure can be increased nearly 2-fold by treatment with a histone deacetylase (HDAC) inhibitor. Using a mouse model of latent HSV infection, we demonstrate that a targeted endonuclease can be delivered to viral latency sites via an adeno-associated virus (AAV) vector, where it is able to induce mutation of latent HSV genomes. These data provide the first proof-of-principle to our knowledge for the use of a targeted endonuclease as an antiviral agent to treat an established latent viral infection in vivo.
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PMID:In vivo disruption of latent HSV by designer endonuclease therapy. 2764 35