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Dissertations / Theses on the topic 'Herpes simplex virus Immuunreacties'

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Published: 4 June 2021
Last updated: 11 February 2022

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1

Ingemarson, Rolf. "Herpes simplex ribonucleotide reductase." Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 1989. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101352.

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In all bacterial, plant and animal cells, as well as in many viruses, genetic information resides in DNA (deoxyribonucleic acid). Replication of DNA is essential for proliferation, and DNA-containing viruses (such as herpesviruses) must carry out this process within the mammalian cells they infect. The enzyme ribonucleotide reductase catalyzes the first unique step leading to the production of the four deoxy-ribonucleotides used to make DNA. Each deoxyribonucleotide is produced by reduction of the corresponding ribonucleotide. After infection of a mammalian cell with herpes simplex virus (HSV) a new ribonucleotide reductase activity appears, which is distinct from the mammalian enzyme activity. This is due to induction of a separate, virally-encoded ribonucleotide reductase. Two monoclonal antibodies were raised against HSV (type 1) ribonucleotide reductase, and were found to bind but not neutralize its enzyme activity. One antibody recognized a larger (140 kD) protein and the other a smaller (40 kD) protein, suggesting the HSV 1 ribonucleotide reductase had a heterodimeric composition similar to that found in many other organisms. The 140 kD protein was sequentially degraded to 110 kD, 93 kD and 81 kD proteins by a host (Vero) cell-specific serine protease. Of these different proteolytic products, at least the 93 kD residue was enzymatically active, suggesting that part of the 140 kD protein may have functions unrelated to ribonucleotide reduction. The 140 and 40 kD proteins bound tightly to each other in a complex of the a2ß2 type, as shown by analytical glycerol gradient centrifugation. An assay system for functional small and large subunits of HSV 1 ribonucleotide reductase was developed, using two temperaturesensitive mutant viruses, defective in either the large (tsl207) or small (tsl222) subunits. Active holoenzyme was reconstituted both in vitro, by mixing extracts from cells infected with either mutant, and in vivo by coinfection of cells with both mutants. The gene encoding the small subunit of HSV 1 ribonucleotide reductase was cloned into an expression plasmid under control of a tac promoter. The recombinant protein was purified to homogeneity from extracts of transfected E. coli, and was active when combined with large subunit, as provided by extracts of tsl222- infected hamster (BHK) cells. The protein contained a novel tyrosyl free radical that spectroscopically resembled, but was distinguishable from, the active-site free radical found in either the E. coli or mammalian small subunits of ribonucleotide reductase. The gene encoding the large subunit of HSV 1 ribonucleotide reductase was also expressed in E. coli, using similar techniques. The recombinant large subunit was immunoprecipitated from extracts of transfected bacteria, and showed weak activity when combined with small subunit, provided by extracts of tsl20-infected hamster (BHK) cells.

Diss. (sammanfattning) Umeå : Umeå universitet, 1989, härtill 4 uppsatser.


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2

Turner, Angelina. "Herpes simplex virus induced membrane fusion." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.625097.

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3

Bajric, Amina. "Validering av Varicella Zoster virus och Herpes Simplex virus." Thesis, Malmö universitet, Fakulteten för hälsa och samhälle (HS), 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-24474.

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Syftet med denna valideringsstudie är att värdera lämpligheten att överföra den manuella analysen av aktuell infektion av Varicella Zoster Virus (aVZV IgM) och Herpes Simplex Virus (aHSV IgM) med SIEMENS Enzygnost® till en av de automatiserade analysinstrumenten EUROIMMUN Analyzer I (ELISA) eller DiaSorin LIAISON® XL. Arbetet utfördes på Klinisk Mikrobiologi i Lund. Konsekutiva serumprover för VZV IgM (n=108) och för HSV IgM (n=116) från det vardagliga flödet analyserades, tillsammans med 10 PCR- eller serokonversion-konfirmerade positiva serumprover av primär infektion VZV och HSV samt 10 positiva för reaktiverad infektion av VZV och HSV. Utöver det användes 10 serumprover konfirmerade positiva för Cytomegalovirus (CMV) respektive 10 för Epstein-Barr Virus (EBV) för att testa korsreaktionen metoderna emellan. Resultatet från VZV-valideringen i Analyzer I samt LIAISON® XL gav en överensstämmelse på 93% respektive 94% av de konsekutiva proverna, 71% respektive 86% av de primärinfekterade proverna och 75% respektive 58% av de reaktiverade proverna, samt en korsreaktivitet (positiva och gränsvärden) på totalt 33% respektive 20% av proverna. Resultatet från HSV-valideringen i Analyzer I samt LIAISON® XL gav en överensstämmelse på 84% respektive 87% av de konsekutiva proverna, 82% respektive 18% av de primärinfekterade proverna och 40% respektive 10% av de reaktiverade proverna, samt en korsreaktivitet (positiva och gränsvärden) på totalt 67% respektive 47% av proverna. Enligt rekommendation efter utförandet av denna studie så bör analysen av HSV IgM uteslutas från båda automatiserade metoder medan VZV IgM bör kontrolleras något ytterligare i Analyzer I, med förhoppning om att denna metod kan vara känsligare.
The approach of this validation study is to evaluate the adequacy for transferring the manual analysis method of ongoing infection of Varicella Zoster Virus (aVZV IgM) and Herpes Simplex Virus (aHSV IgM) with SIEMENS Enzygnost® to one of the automated instruments EUROIMMUN Analyzer I (ELISA) or DiaSorin LIAISON® XL. The study was carried out at Clinical Microbiology in Lund. Consecutive serum samples for VZV IgM (n=108) and HSV IgM (n=116) from the daily local flow of tests were analyzed, along with 10 positive for primary infection of VZV and HSV, confirmed by PCR or seroconversion, and 10 with reactivated infection of VZV and HSV. Beyond those, 10 serum samples confirmed positive for Cytomegalovirus (CMV) respectively 10 for Epstein-Barr Virus (EBV) to test the cross-reaction between the three methods. The results from the validation of VZV in Analyzer I and LIAISON® XL gave an agreement of 93% and 94% respectively in the consecutive tests, 71% and 86% respectively in the primary infected tests and 75% and 58% respectively in the reactivated tests, and also a cross-reactivity (both positive and in between-values) at a total of 33% respectively 20% of the tests. The results from the validation of HSV in Analyzer I and LIAISON® XL gave an agreement of 84% and 87% respectively in the consecutive tests, 82% and 18% respectively in the primary infected tests and 40% and 10% respectively in the reactivated tests, and also a cross-reactivity (both positive and in between-values) at a total of 67% respectively 47% of the tests. According recommendations after the performance of this study, the analysis of HSV IgM should be excluded from both of the automated methods while VZV IgM should be controlled further in Analyzer I, with hopes that this new method could be more sensitive.
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4

Atfield, Rachel Sarah. "Herpes simplex virus glycoprotein-mediated membrane fusion." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615860.

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5

Nahum, Joseph. "Thérapeutique des infections à Herpes simplex virus." Paris 5, 1999. http://www.theses.fr/1999PA05P200.

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6

Graham, Richard Peter. "Purification of glycoproteins from herpes simplex virus." Master's thesis, University of Cape Town, 1985. http://hdl.handle.net/11427/25694.

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The aim of this work was to purify type-specific glycoproteins from herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) for diagnostic use. The most likely candidate for a type-specific glycoprotein of HSV-1 is glycoprotein C (gC), although it has recently been shown to contain some type-common antigenic determinants. HSV-1 and HSV-2 were produced in BHK-21 cells and labelled with either (³H)-glucosamine ((³H)-gln) or a mixture of (¹⁴C)-amino acids ((¹⁴C)-aa). Analysis of the radiolabelled products by analytical sodium dodecyl sulphate polyacrylamide gel electrophoresis (SOS-PAGE) and autoradiography revealed that in the HSV-1 infected cells the radiolabelled components were incorporated into viral specific proteins only, whereas in the HSV-2 infected cells they were incorporated into host cell proteins as well as viral proteins. Preparative polyacrylamide gel electrophoresis (Prep-PAGE) was used as an initial step in separating HSV-1 infected cell proteins labelled with (³H)-gln. Two cycles of Prep-PAGE were sufficient to produce solutions containing either glycoprotein B ( gB) or glyco- protein C (gC), which were free of other HSV-1 glycoproteins. However, these solutions still contained a number of non-glycosylated proteins. Two different techniques were utilized to remove the non-glycosylated proteins from the glycoprotein solutions. Hydroxylapatite (HAUltrogel) chromatography in the presence of sodium dodecyl sulphate (SDS-HTP) did not separate the different HSV-1 glycoproteins and was not satisfactory for removing the non-glycosylated proteins. Gel-bound lectin affinity chromatography using wheat germ lectin and Helix pomatia lectin was not successful in purifying the glycoproteins because the glycoproteins which bound to the lectins could not be eluted under normal conditions. Difficulties encountered in eluting the HSV-1 glycoproteins from the lectins may have been due to the sodium dodecyl sulphate (SOS) in which the proteins were solubilized. For this reason, the gelbound lectin affinity chromatography was repeated using HSV-1 membrane proteins solubilized in a non-ionic detergent, Triton X-100. Using material prepared in this way, several HSV-1 glycoproteins were bound by wheat germ lectin and eluted under normal conditions to yield glycoproteins which were purified with respect to nonglycosylated proteins.
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7

Barr, Beverly Bell Brown. "Molecular epidemiology of herpes simplex virus infections." Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/19152.

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8

Delboy, Mark. "PROTEASOME-DEPENDENT ENTRY OF HERPES SIMPLEX VIRUS." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/47.

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Herpes simplex virus entry into cells is a multistep process that engages the host cell machinery. The proteasome is a large, ATP-dependent, multisubunit protease that plays a critical role in the maintenance of cell homeostasis. A battery of assays were used to demonstrate that proteasome inhibitors blocked an early step in herpes simplex virus entry that occurred after capsid penetration into the cytosol but prior to capsid arrival at the nuclear periphery. Proteasome-dependent viral entry was not reliant on host or viral protein synthesis. MG132, a peptide aldehyde that competitively inhibits the degradative activity of the proteasome, had a reversible inhibitory effect on herpes simplex virus capsid transport. Herpes simplex virus can use endocytic or nonendocytic pathways to enter cells. These distinct entry routes were both dependent on proteasome-mediated proteolysis. In addition, herpes simplex virus successfully entered cells in the absence of a functional host ubiquitin-activating enzyme, suggesting that viral entry is ubiquitin independent. Herpes simplex virus immediate-early protein ICP0 is a multifunctional regulator of herpes simplex virus infection. Late in infection ICP0 interacts dynamically with cellular proteasomes. ICP0 has a RING finger domain with E3 ubiquitin ligase activity that is necessary for its IE functions. The fundamental and functional properties of ICP0 that is present in the virion tegument layer have not been well characterized. For these reasons, I sought to characterize tegument ICP0 and determine the role of tegument ICP0 during proteasome-dependent entry of herpes simplex virus. Protein compositions of wild-type and ICP0 null virions were similar, suggesting that the absence of ICP0 does not grossly impair virion assembly. Virions with mutations in the RING finger domain contained greatly reduced levels of tegument ICP0, suggesting that the domain influences the incorporation of ICP0. Virion ICP0 was resistant to removal by detergent and salt and was associated with capsids, features common to inner tegument proteins. ICP0 mutations that resulted in the absence of ICP0 in the tegument layer, allow herpes simplex virus to enter cells independently of the proteasome activity. I propose that proteasomal degradation of virion and/or host proteins is regulated by ICP0 to allow for efficient delivery of incoming herpes simplex virus capsids to the nucleus.
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9

Dambrosi, Sarah. "Neurovirulence et latence des virus Herpes simplex mutants." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26368/26368.pdf.

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10

Whiteley, Alison. "Studies of herpes simplex virus type-1 envelopment." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621703.

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11

Wu, Zetang. "Silencing Suppression by Herpes Simplex Virus Type 1." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1213287215.

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12

Kogishi, Junichi. "Mutant herpes simplex virus-mediated suppression of retinoblastoma." Kyoto University, 1999. http://hdl.handle.net/2433/181258.

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13

Ewing, Stephen Michael George. "Herpes simplex virus type 1 infection of dendritic leucocytes." Thesis, University of Oxford, 1992. http://ora.ox.ac.uk/objects/uuid:e83750b1-3aa7-452e-a876-be51690252be.

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14

Hodge, Paul Daniel. "The encapsidation of herpes simplex virus type 1 DNA." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301951.

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15

Johnson, Paul Andrew. "The control of herpes simplex virus late gene transcription." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481097.

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16

McBride, Brian William. "Mucosal immune responses induced by herpes simplex virus infection." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254770.

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17

Stumpf, Thomas Hugo. "Immunopathology of herpes simplex virus infections in the eye." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250985.

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18

Atkinson, Helen Ruth. "Molecular studies of herpes simplex virus type 1 latency." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241568.

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19

Hedner, Ewa. "Herpes Simplex virus type 1 and intraoral wound healing." [Göteborg] : Departments of Clinical Virology, Faculty of Medicine, Oral Microbiology and Oral Surgery, Faculty of Odontology, University of Göteborg, 1993. http://catalog.hathitrust.org/api/volumes/oclc/30761199.html.

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20

Harman, Laura Emily Rose. "Immunological control of herpes simplex virus type 1 latency." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708822.

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21

Svobodová, Stanislava. "Study of herpes simplex virus type 1 tegument assembly." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607957.

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22

Stoner, Terri Dorene. "Indole-3-Carbinol Inhibition of Herpes Simplex Virus Replication." Kent State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=kent1228328838.

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23

Naldinho, Souto Raquel Cristina. "Studies of Herpes Simplex Virus type-1 tegument proteins during virus egress." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613035.

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24

Rajaguru, Suesha Chandani. "Inhibition of herpes simplex virus replication using small interfering rna that target icp4 gene of herpes simplex type 2." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0007066.

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Thesis (M.S.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 65 pages. Includes Vita. Includes bibliographical references.
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25

Striebinger, Hannah. "Membran-assoziierte Protein-Protein-Interaktionen des Herpes simplex-Virus 1." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-146882.

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26

Brown, Elizabeth L. "Consequences of genital herpes simplex virus infection among vulnerable populations /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10885.

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27

Littlejohn, Emma Sophie Vout. "The Sensitivity of Adenovirus and Herpes simplex virus to Honey." The University of Waikato, 2009. http://hdl.handle.net/10289/2804.

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Honey has been used for centuries as a medicine to treat various ailments and infections. A large amount of research has established that honey has potent antibacterial activity. However, the sensitivity to honey of viral species that cause infections has been studied in only a small number of cases. The aim of this study was to obtain data to clarify and extend knowledge obtained from these previous studies of honey's antiviral activity, and especially study those viruses that cause localised infections which have limited or no therapy available, which are suitable to treatment with topically applied honey. The susceptible A549 cell line and viral isolates of Adenovirus serotypes 1, 3, and 8, and Herpes simplex virus serotypes 1 and 2, were provided by the Waikato Hospital Virology Laboratory. A number of types of honey were investigated from a range of sources: Manuka honey with high concentrations of methylglyoxal, unique manuka factor activity, and phenolics, Honeydew and Rewarewa honeys which have high antioxidant activity, and Ling Heather honey which is high in phenolic compounds. These honeys were selected due to their range of characteristic activities in order to make comparisons with antiviral activity. A variety of tests using cell culture were developed to evaluate the sensitivity of the viruses to whole honey. Each test scored and monitored the development of morphological changes to the cells, to observe whether the honey treatment can prevent the development of these changes known as viral cytopathic effect. These included tests for: protection, in which the cells were pre-treated with, and iii incubated either with or without honey; prevention, where honey was used to treat infected cells, and in plaque reduction assays, to examine whether it can reduce the resultant number of plaques; and neutralisation, in which the virus was directly exposed to the honey for a defined period. It was found with each type of test using cell culture that many of the honeys studied can lower the severity of viral cytopathic effect or delay its onset compared with the development observed with virus that was not treated with honey. This can suggest that the antiviral activity may be a feature of more than one type of honey. In general the antiviral effect increased with the concentration of honey and time the virus was exposed to it. Manuka honey M116 at a concentration of 10% was effective in preventing the development of viral cytopathic effect of each of virus, after the viruses at concentrations in excess of the tissue culture infectious dose had been exposed to the honey for 8 hours. Enzyme-linked immunosorbant assays were used to measure the effect the successful treatments found in the extended neutralisation experiments had on viral surface proteins necessary for viral entry into the cells. The results using this technique suggested that there was very little virus present in the samples that had been treated with honey and with the untreated virus. Therefore it could not be shown whether the honey was acting via this mechanism. It is concluded from the findings in this study that honey is likely to be an effective antiviral treatment for the therapy of localised viral infections, this needs to be verified by clinical trials.
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28

Szerwinski, Anne [Verfasser]. "Szientometrische Analyse der Bedeutung des Herpes simplex Virus / Anne Szerwinski." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024864758/34.

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29

McGeehan, John Edward. "Molecular characterisation of Herpes simplex virus type 1 deoxyuridine triphosphatase." Thesis, University of Glasgow, 1998. http://theses.gla.ac.uk/6104/.

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Analysis of primary sequence data revealed a subset of open reading frames that were predicted to encode HSV-I dUTPases based on five areas of local primary sequence conservation. The differences in the primary sequence organisation of these motif regions allowed the description of two distinct dUTPase classes. The class I dUTPases are encoded by a diverse range of organisms and are characterised by a trimeric arrangement with subunit protein lengths approximating 150 amino acids. The class II dUTPases are specific to the herpesviruses and are characterised by a monomeric arrangement with a protein chain length approximately double that of their class I counterparts. It has been proposed that the class II dUTPases arose by the intragenic duplication of the class I open reading frame. In this thesis the class I structures were used as a basis to investigate the HSV-1 class II dUTPase in terms of structural and evolutionary relationships. To allow a defined approach to functional analysis of the HSV-1 dUTPase a tertiary structural model was generated for the class II enzymes. Following intensive primary sequence analysis a method was devised for comparing class I and class II sequences directly. Secondary structure prediction programs were utilised to judge the basic structural similarities between the two classes allowing the proposition of several defined hypotheses. The available class I structural information was utilised in order to characterise highly conserved structural elements within the class I group. In was then possible to relate this data set to class I primary sequences and subsequently to the generation of a class II model. Various modelling techniques were used based on the constraints on the structural organisation that could achieve a functionally active monomer plus the set of hypotheses defined in the earlier work. Mutagenic analysis of the HSV-1 dUTPase was then possible using the class II model as a reference. Several targets were investigated based on predicated functionally important regions. Analysis of these mutant enzymes was performed using purified recombinant HSV-1 dUTPase expressed from the T7 E.coli expression system.
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30

Orzalli, Megan Jenkins. "Inhibition of Nuclear DNA Sensing by Herpes Simplex Virus 1." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10779.

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The detection of immunostimulatory DNA is well documented to occur at several cellular sites, but there is limited evidence of nuclear innate DNA sensing. Prior to this study, the detection of herpesviral DNA was thought to be restricted to the cytosol so as to limit the sensing of host DNA in the nucleus. However, given the nuclear lifecycle of these viruses, we hypothesized that viral DNA could be sensed in the nucleus of infected cells. To test this hypothesis we examined the activation of interferon regulatory factor 3 (IRF-3) in response to herpes simplex virus 1 (HSV-1) infection of primary human foreskin fibroblasts (HFF). Using a mutant defective for expression of all viral genes, we observed that the release of viral DNA into the nucleus is necessary to activate IRF-3 signaling. Furthermore, we determined this response to be dependent on nuclear-localized interferon inducible protein 16 (IFI16) and the cytoplasmic stimulator of interferon genes (STING) adaptor protein.
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31

Porter, Iain Malcolm. "Characterisation of the herpes simplex virus type 1 mutant, ambUL12." Thesis, University of Glasgow, 2002. http://theses.gla.ac.uk/3959/.

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The herpes simplex virus type 1 (HSV-1) UL12 gene encodes an alkaline nuclease. Although the UL12 gene is not absolutely essential for replication, UL12 null mutants produce 100-1000 fold less viable virus than wt HSV-1. It has been suggested that the alkaline nuclease functions to remove branched structures from high molecular weight concatemeric DNA prior to its cleavage into monomeric genomes that are packaged into viral capsids. Failure to remove the branches results in unstable packaging of DNA into capsids which fail to egress from the nucleus. This thesis describes detailed characterisation of the HSV-1 mutant, ambUL12 (Patel et al., 1996) which fails to express the alkaline nuclease due to the insertion of an amber stop codon into the UL12 open reading frame. The ability of ambUL12 to replicate and package both viral genomic DNA and amplicons (plasmids containing the HSV-1 origin of replication and DNA encapsidation signal) was examined. In contrast to results obtained with other alkaline nuclease mutants, which replicate and package DNA with close to wt HSV-1 efficiency (Shao et al., 1993; Martinez et al., 1996b), ambUL12 displayed a 3-5 fold drop in replication and a 15-20 fold drop in packaging of genomic DNA. Similar reductions were observed in the replication and packaging of amplicon DNA. The replication and packaging of amplicons by ambUL12 in these transient assays could be partially complemented when UL12 was supplied in trans. Close inspection of the DNA molecules synthesised during transient assays demonstrated that amplicon replication intermediates are complex high molecular weight concatemers that undergo intermolecular recombination, analogous to viral DNA replication intermediates.
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32

Dalrymple, M. A. "The regulation of herpes simplex virus immediate early gene expression." Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378173.

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33

Preetha, Balan K. V. "Analysis of dispensable glycoproteins of herpes simplex virus type 1." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320012.

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34

Görander, Staffan. "Functions of glycoprotein G of herpes simplex virus type 2." Göteborg : Dept. of Infectious Medicine, Section for Virology, Sahlgrenska Academy, 2010. http://hdl.handle.net/2077/21861.

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35

Galdiero, Massimiliano. "Mutagenesis of glycoprotein H of herpes simplex virus type 1." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624784.

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36

Jenkins, Mary K. "Metabolism of Herpes Simplex Virus 1 infected RAW 264.7 macrophages." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1472203113.

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37

Doll, Jessica R. "Insights into Herpes Simplex Virus Pathogenesis: Neuronal Fate Post-Reactivation." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535458248721271.

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38

Sayers, Charlotte. "Herpes simplex virus type 1 infection of human keratinocyte cells." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11112.

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Infection of herpes simplex virus type 1 (HSV-1) begins at the epidermis, a stratified layer composed primarily of keratinocytes. The physiologically relevant cell type for the study of HSV-1 assembly is therefore the human keratinocyte. Nonetheless, relatively little is known about the replication of HSV-1 in this natural host cell. Comparison of virus growth in monolayers of keratinocyte cells and Vero cells, a routinely used cell line for HSV-1 studies, revealed that these keratinocytes support a more productive virus replication than Vero cells. Furthermore, newly assembled virus is produced more rapidly in keratinocytes and this enhancement occurs prior to, or upon the initiation of immediate early gene transcription. This augmented replication in keratinocytes can be at least partially attributed to the method of entry of the virus. We have found by penetration assays and electron microscopy that the virus is able to penetrate keratinocyte cells much more rapidly than Vero cells. We have also shown that the virus entry mechanism is more efficient at lower temperatures in nTERT cells, with virus entering cells at temperatures as low as 7°C. Additionally preliminary work implies that depletion of one of the herpes virus entry receptors, Nectin-1, does not affect entry into nTERT cells, whereas entry is reduced up to 65% in HeLa cells. Taken together, these results imply a role for other entry receptors, possibly as yet unidentified, in the entry of human keratinocyte cells. This work also identifies a role for cellular Rab proteins, GTPases essential for the regulation of vesicle trafficking, in HSV-1 infection of keratinocytes. In particular Rab6, which was also found to play a role in infected HeLa cells (Elliott Group), appears to have a similar function in both these cells and together support a model for HSV-1 morphogenesis involving Rab-regulated vesicle trafficking of viral glycoproteins to the cell surface. Several other Rabs identified by this screen now provide interesting opportunities to elucidate further roles of Rab proteins in HSV-1 infection of keratinocyte cells. This project has broadly characterised the replication of HSV-1 in keratinocyte cells and explored the role of Rab GTPases in virus trafficking within keratinocytes - a cell type that is physiologically relevant to infection.
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39

Zhou, Amy Yuan. "Exploring the functional role of herpes simplex virus type-1 glycoprotein H in virus entry." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648658.

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40

Teepe, Annette. "Relationship of Estrous Cycle to Herpes Simplex Virus Type 2 Susceptibility in Female Mice." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc500408/.

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In CBA/NJ mice, splenic natural killer (NK) cell activity varies with stages of estrous. Susceptibility of ICR mice to intravaginal inoculation of herpes simplex virus type 2 (HSV-2) decreases with age. Susceptibility of female ICR and CBA/NJ mice to HSV-2 inoculated intravaginally and intraperitoneally was examined during the estrous cycle. In cycling ICR mice, greatest susceptibility to intravaginal inoculation was observed during diestrous and the least during metestrous. CBA/NJ mice were most susceptible to intravaginal inoculation of HSV-2 during diestrous. ICR mice were ovariectomized to mimic diestrous and found to be highly susceptible to intravaginal inoculation at all virus doses. No difference in susceptibility among phases of the estrous cycle was seen following intraperitoneal inoculation.
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41

Schelhaas, Mario. "Untersuchungen zu Eintrittsmechanismen des Herpes simplex-Virus Typ 1 in Epithelzellen." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970871333.

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42

Stavropoulos, Tom Anastasios. "An enhanced packaging system for helper-dependent herpes simplex virus vectors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/MQ58088.pdf.

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43

Bunnell, Scott Morris. "Characterization of unexpected ICP27 recombinants and revertants of herpes simplex virus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ60280.pdf.

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44

Wang, Yisheng. "Characterizations of DNA replication proteins from herpes simplex virus type 1." Diss., The University of Arizona, 1990. http://hdl.handle.net/10150/185295.

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This study was designed to characterize two DNA replication proteins from herpes simplex virus type 1 (HSV-1): the major DNA binding protein (ICP8) and the DNA polymerase. The two proteins are among the seven proteins required for viral DNA synthesis. Four areas were investigated. First, the ICP8 protein was purified from an overproducing cell and showed to behave the same as the viral protein in interacting with DNA. To define the DNA-binding domain of the protein, a proteolytic fragment with the same DNA-binding specificity as the intact protein was identified by a protein blotting assay. N-terminal protein sequencing located the fragment between residues 300 and about 849 in the intact protein. This fragment contains some features important for DNA binding. Second, the DNA polymerase was found to replicate non-processively in vitro. The ICP8 protein slightly stimulated the polymerase activity at lower concentrations and inhibited its activity as the ICP8 concentration increased. Third, to define the functional domain of the DNA polymerase, a fragment of the polymerase predicted to contain both the polymerase and 3$\sp\prime$-5$\sp\prime$ exonuclease activities was overexpressed in Escherichia coli. The fragment was partially purified and its enzymatic activity was examined. Finally, to identify polymerase residues involved in substrate binding, three amino acid changes in polymerase mutants with altered drug sensitivities have been identified by DNA sequencing. Two mutations, affecting nucleotide binding, occur near two highly conserved regions which constitute part of a putative nucleotide binding site. This result indicates that two more residues are important for substrate binding. The third mutation, affecting pyrophosphate binding, occurs upstream of any previously known mutations. This result may indicate a new region involved in substrate binding.
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45

Baker, Robert Owen. "Cellular factors involved with, and fidelity of herpes simplex virus replication." Diss., The University of Arizona, 1999. http://hdl.handle.net/10150/284045.

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Herpes Simplex Virus type 1 is an important organism not only because it is a member of a family of disease-causing organisms, but it also serves as a model organism for the study of eukaryotic DNA replication. Here I use HSV-1 to investigate two aspects of DNA replication: initiation and proofreading. Cellular factors have been shown to be involved in DNA replication, and especially in initiation, in a variety of viral systems. Previous studies have identified the first cellular factor implicated in initiation of HSV-1 replication, OF-1. In this study, I have purified OF-1 and investigated its composition, binding properties and interactions with the viral origin binding protein UL9. I show that OF-1 is composed of two subunits, one of which contains DNA binding activity. I also found that OF-1 binds specifically to both single- and double-stranded origin DNA, that OF-1 binds most tightly to single-stranded DNA, and that OF-1 shows a preference for which strand is bound. I have demonstrated that, in the presence of UL9, OF-1 exhibits a higher affinity for its target DNA and that OF-1 inhibits the ATPase activity of UL9. I propose that UL9 binds to the origin of replication, loads OF-1 to the origin, and then is displaced by OF-1. Further implications for this model are discussed. I go on to investigate several aspects of error control in the wild type and a 3'-5' proofreading exonuclease mutant DNA polymerase from HSV-1. Proofreading is a primary factor influencing the fidelity of DNA replication. Previous studies in our lab have shown that exonuclease deficient polymerases are incapable of supporting viral growth in vivo. In these studies, I have expressed and purified both wild type and mutant polymerases and investigated their biochemical properties as well as the mechanism of lethality of the mutant. I have found that the mutant polymerase exhibits substantially elevated rates of nucleotide misincorporation as compared to the wild type. In addition, the mutant polymerase is seen to stall at a misincorporation, exhibiting a reduced ability to replicate past a mismatch. Based on these findings, I suggest that the inability of the mutant polymerase to replicate past a misinsertion is the primary cause of the reduced viability of viruses carrying the mutant enzyme.
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46

English, Christie. "Molecular characterisation of the Herpes Simplex Virus-1 LATP2 enhancer region." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444664/.

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HSV1 vectors have previously been produced with the ability to direct long-term expression of a transgene within the nervous system. These viruses have an arrangement of the latency promoter and enhancer regions LAP1 and LATP2 such that LATP2 exerts long-term expression onto LAP1 and an exogenous promoter at the same time, in a back-to-back fashion. To characterise the LATP2 region, two series of vectors were produced containing deletion mutations of the region placed in different orientations to LAP1 within the context of the original vectors. The vectors were tested in vitro and in vivo in the PNS and a potentially repressive region within LATP2 was identified. The enhancer activity of the region was also localised to a defined area. As the HSV1 genome is associated with histones and modification of these is a method of transcriptional control, histone modification could be one mechanism that the virus uses to keep the LAT region active during latency. This was investigated by examining the acetylation of histones associated with the LAT region, including LATP2, at lytic and latent timepoints in an in vitro system by ChIP assay. These studies found that although no significant differences in acetylation at different loci of LATP2 was found, the LAT regulatory region generally appears to be more associated with hyperacetylated histones during latency than non-LAT promoters and that this increased acetylation is conferred onto an exogenous promoter when placed within the LAT region. The findings in this thesis should provide insight into the functioning of the LAT region and may allow the development of improved HSV1 vectors for gene therapy in the nervous system.
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47

Grey, F. E. "Investigation of factors involved in herpes simplex virus type 1 pathogenesis." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599699.

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The mouse model has been extensively used in studies of HSV pathogenesis and has led to a greater understanding of many aspects of the virus life cycle and viral replication in vivo. The current study makes use of the mouse model to investigate two aspects of viral pathogenesis. The initial project concerns viral resistance to the antiviral drug Aciclovir (ACV) and the pathogenesis of a resistant clinical isolate. The aim of the second project was to investigate the effects of disrupting antigen presentation by MHC class I on the replication and pathogenesis of HSV-1. Aciclovir is a highly effective drug in the treatment of herpetic infections. Its effectiveness, however, is undermined by the emergence of resistance virus isolates that can cause serious disease in immunocompromised patients. In the majority of cases resistance occurs through a mutation that disrupts the TK gene of HSV and is normally associated with attenuation of neurovirulence. In this study a clinical isolate resistant to ACV (4B) was found to display a high level of neurovirulence despite a double G insertion mutation that would theoretically disrupt all TK activity. Following inoculation of the mice the virus was able to replicate efficiently in dorsal root ganglia during acute infection and was able to reactivate from latency. Furthermore, plaque purified isolates of 4B uniformly expressed a very low level of TK activity. Disruption of the TK gene of 4B led to a loss of the low level of TK activity and a loss in the ability to replicate in the ganglia of mice and to reactivate from latency. Further investigation showed that the ability of isolate 4B to replicate in the nervous system of mice was due to the virus gaining an additional G residue, rescuing the original frameshift mutation and allowing the virus to express wild type levels of TK. The neurovirulence associated with 4B is therefore due to phenotypic reversion. The immune response of the host plays an important role in shaping the pathogenesis of HSV. To counteract the antiviral effects of the immune system HSV encodes a number of genes involved in immune evasion.
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48

Adamson, Walt Eric. "Mapping the proteins of the herpes simplex virus type 1 capsid." Thesis, University of Glasgow, 2006. http://theses.gla.ac.uk/3963/.

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The aims of the work presented in this thesis were to use a variety of mutagenesis techniques to investigate the proteins of the HSV-1 capsid. Triplexes are heterotrimers formed by two proteins in a 1:2 stoichiometry. The single-copy protein is called VP19C, and the dimeric protein is VP23. Insertional and deletional mutagenesis was carried out on VP19C and the effects of the mutations on virus growth and capsid assembly were examined. Insertional mutagenesis showed that VP19C can be divided into three regions with respect to their ability to tolerate five amino acid insertions, with two regions of approximately 100 amino acids at the N- and C-terminal regions of the protein being more tolerant of such insertions than a ~350 amino acid central region. The N-terminal ~100 amino acids of the protein, which are particularly insensitive to insertional mutagenesis, correspond to a region that is poorly conserved among herpesviruses. Some, but not all, severely disabled mutants were compromised in their ability to bind VP23 and VP5. Analysis of deletional mutants revealed the presence of an unusual nuclear localisation signal (NLS) near the N-terminus of VP19C. This was mapped to a 33 amino acid region by fusion of specific sequences to a green fluorescent protein (GFP) marker. By replacing the endogenous NLS with that from the simian virus 40 (SV40) large T antigen, we were able to show that the first 45 amino acids of VP19C were not essential for assembly of functional capsids and infectious virus particles. However, removing the first 63 amino acids resulted in the formation of aberrant capsids and prevented virus growth, suggesting that the poorly-conserved N-terminal sequences have some as-yet-unidentified function.
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49

Vaughan, P. J. "Studies on a component of the herpes simplex virus DNA polymerase." Thesis, University of Leeds, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379648.

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50

Robinson, Michael James. "Development of herpes simplex virus vectors with a neuronal-specific promoter." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313298.

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