Dissertations / Theses: 'Herpes simplex virus'

1

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

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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. digitalisering@umu

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3

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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4

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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5

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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6

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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7

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

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13

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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14

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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15

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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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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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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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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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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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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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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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

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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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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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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26

Denes, Christopher. "Virus-host interactions of herpes simplex virus type-1 envelope glycoprotein E." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23098.

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Herpes simplex virus type-1 (HSV-1) lays dormant in approximately 67% of individuals worldwide. The typical orolabial or genital lesions are relatively innocuous, but infection can cause encephalitis and systemic infections in susceptible populations. With no vaccine available, research into new antivirals is critical for managing the increasing incidence of antiviral resistance as well as the impact of virus shedding events. One approach to the discovery of new antivirals is the identification of host-pathogen interfaces necessary for viral replication and spread. Glycoprotein E (gE) is an HSV-1 envelope protein important for viral egress and cell-to-cell spread. In this study, we identified the global gE interactome in epithelial HeLa and neuron-like differentiated SH-SY5Y cell lines as representative cell types of the binary nature of natural herpes infection. Validation of these findings confirmed a functional interaction between gE and the adaptor protein 2 (AP-2) complex that regulates gE endocytosis via a tyrosine sorting motif region within the gE cytoplasmic tail (CT). We also identified interactions between gE and the Rab GTPases Rab7A and Rab11A. Rab7A likely directs gE to sites of envelopment while Rab11A may facilitate delivery of vesicle-wrapped mature virions to the plasma membrane through its interaction with gE. Separately, based on motif searching and preliminary data, we observed an interaction between gE and the WAVE Regulatory Complex (WRC). This interaction is not dependent on an interaction domain within the gE(CT) termed the WRC Interacting Receptor Sequence, and this stretch of amino acids does not contribute to release and spread of the virus, either. Whether these interactions are direct or formed by bridging complexes is yet to be determined but given that our work represents some of the first specific gE/host interactions found, it will likely pave the way to the discovery of one or more new antiviral targets.

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27

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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28

Williams, N. A. "The role of Langerhans cells in infection with herpes simplex virus." Thesis, University of Bristol, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235240.

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Liu, Lei. "Immunology of herpes simplex keratitis and its treatment by corneal transplantation." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources. Online version available for University member only until Sep. 7, 2010, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=33585.

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30

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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31

Liu, Mingyu. "Gene regulation and function of ICP0 in herpes simplex virus infected cells." OpenSIUC, 2010. https://opensiuc.lib.siu.edu/dissertations/143.

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Herpes simplex virus (HSV) is a clinically important virus, whose life cycle alternates between productive replication and latency. Infected cell protein 0 (ICP0) is generally believed to play a key role in determining the outcome of HSV infections. Synthesis of ICP0 promotes the productive replication of HSV, whereas absence of ICP0 renders HSV prone to establish latent infections. In the first part of the dissertation, I attempt to address the question how is ICP0 gene regulated. To tackle this question, we constructed recombinant HSV that encodes GFP-tagged ICP0 so that the regulation of ICP0 gene can be visualized in real time. Using this reagent, we found that ICP0 gene was subject to potent repression immediately following infection. Surprisingly, HSV's major transcriptional regulator, ICP4, was necessary and sufficient to repress ICP0 gene, and did so in an ICP4-binding-site dependent manner. Synthesis of ICP0 alleviated the ICP4-dependent repression of ICP0 gene. ICP4 co-immunoprecipitated with FLAG-tagged ICP0, thus, a physical interaction between ICP0 and ICP4 likely explains how ICP0 antagonizes ICP4's capacity to silence the ICP0 gene. Therefore, our findings suggest that ICP0 gene is differentially regulated by virus-encoded repressor ICP4 and virus-encoded antirepressor ICP0. In the second part of the dissertation, I attempt to address the question what function does ICP0 assume. Since the discovery of ICP0, the nuclear function of ICP0 has been the focal point of studies, whereas the cytoplasmic function of ICP0 is unknown. While pursuing our first study, we unexpectedly found that GFP-tagged ICP0 was predominantly localized to the cytoplasm during infections. Taking advantage of live-cell imaging, we found that ICP0 translocated from nucleus to cytoplasm during early phase of HSV infections, where it bundled and dispersed microtubules. Synthesis of ICP0 was proved to be necessary and sufficient to dismantle microtubules in HSV-infected and transfected cells. Therefore, our findings suggest ICP0 might play a previously unrecognized role in the cytoplasm through dismantling microtubule networks of the host cells. Furthermore, our study represents the first report showing a virus-encoded E3 ligase disrupts host cell microtubule networks, thus suggests a general function of many other viral E3 ligases.

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Cheung, Peter. "Brefeldin A arrests the maturation and egress of herpes simplex virus particles during infection." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/29798.

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Herpes Simplex Virus (HSV) requires the host cell secretory apparatus for the maturation and egress of newly synthesized viral particles. Not only do viral glycoproteins rely on the host ER and Golgi compartments for their proper processing, it is believed that enveloped particles are transported through these same organelles for their export out of the cells. Brefeldin A (BFA) is a compound that induces retrograde movement of material from the Golgi apparatus to the ER and causes the disassembly of the Golgi complex. In this study, the effects of BFA on the propagation of HSV-1 in infected cells were examined. Release of viral particles from infected cells was inhibited by as little as 1 µg/ml BFA. Further analysis revealed that BFA did not affect the normal assembly of viral nucleocapsids, but did block the movement of newly-enveloped particles from the nucleus into the cytoplasm. Naked nucleocapsids were found in the cytoplasm of infected cells treated with BFA, however, these particles were neither infectious, nor were they released from the cells. Although BFA altered the distribution of viral glycoproteins in infected cells, this alteration was reversed within 2 hours after the removal of BFA. In contrast, the BFA-induced blockage to viral release was not fully reversed after BFA was removed and cells were allowed to recover in fresh medium for 3 hours. These findings indicate that the BFA-induced retrograde movement of material from the Golgi complex to the ER early in infection arrests the ability of the host cell to support the maturation and egress of enveloped viral particles. Furthermore, exposure of infected cells to BFA during the exponential release phase of the viral life cycle can cause irreversible damage to the egressing particles. This suggests that productive growth of HSV-1 in infected cells relies on a series of events that, once disrupted by agents such as BFA, cannot be easily reconstituted. Science, Faculty of Microbiology and Immunology, Department of Graduate

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Grapes, Matthew Giles Robert. "Analysis of transcriptional activation by the HSV-1 protein VP16 and its EHV-1 homologue." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325048.

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Kew, Chun, and 喬駿. "Inhibition of PACT mediated type 1 interferon production by herpes simplex virus type 1 Us11 protein." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206481.

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Mammals have complicated antiviral innate immunity to combat viral infection and this poses a strong selection pressure on the viruses. As a result, many viruses have evolved different strategies to disrupt the function of hosts’ antiviral innate immunity. Herpes simplex virus type 1 (HSV-1) is one of the examples. HSV-1 is a common and important human pathogen. HSV-1 infection induces type I interferons (IFNs) which restrict viral replication potently. To ensure persistent infection and successful replication, HSV-1 encodes several IFN-suppressing proteins. One example is Us11. Interaction between Us11 and various cellular proteins, such as PKR, RIG-I and PACT, were shown by other studies. However, exactly how Us11 suppresses IFN function remains to be elucidated. In this study, I discovered that Us11 specifically inhibits PACT induced activation of RIG-I. In HSV-1 infected cells, PACT and Us11 associate with each other tightly and this interaction prevents the interaction of PACT with RIG-I. It was also found that RNA binding domains on both PACT and Us11 are important for the association. In infection experiments, the increased production of IFN- during the infection of PACT-competent cells with Us11-deficient HSV-1 recombinant virus was not observed in infected PACT-compromised cells, suggesting the requirement of PACT for Us11 suppression of IFN production. To conclude, this study provides an explanation for Us11 antagonism of IFN production. My findings suggest that PACT is a novel target of HSV-1 IFN-antagonizing protein Us11. published_or_final_version Biochemistry Master Master of Philosophy

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35

Targett-Adams, Paul. "Characterisation of the HSV-1 DNA packaging protein encoded by the UL25 gene." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368523.

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36

Leslie, Jenny. "An investigation into factors that influence the incorporation of proteins into the HSV-1 tegument." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297029.

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Manickasingham, Shrivanthi Prithiva. "The effects on Langerhans cells and dermal leukocyte populations of agents which trigger herpes simplex reactivation." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337696.

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Pawliczek, Tobias. "Studies on the role of the cellular ESCRT machinery in herpes simplex virus type 1 replication." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609315.

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Nicoll, Michael Peter. "The role of the Herpes simplex virus type 1 latency-associated transcripts during the establishment and maintenance of latency." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607713.

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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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41

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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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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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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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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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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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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47

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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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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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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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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Dissertations / Theses on the topic 'Herpes simplex virus'

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