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A study of the effects of herpes simplex virus on cultured human cellsHinze, Harry Clifford, January 1958 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1958. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 80-85).
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Membrane proteins of herpes simplex virus infected cells immunological and biochemical studies /Welling-Wester, Sijtske. January 1981 (has links)
Thesis (doctoral)--Rijksuniversiteit te Groningen.
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Identification and analyses of a herpes simplex virus type 1 glycoproteinGompels, V. A. January 1986 (has links)
No description available.
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The effects on Langerhans cells and dermal leukocyte populations of agents which trigger herpes simplex reactivationManickasingham, Shrivanthi Prithiva January 1996 (has links)
No description available.
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The role of Langerhans cells in infection with herpes simplex virusWilliams, N. A. January 1989 (has links)
No description available.
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Analysis of transcriptional activation by the HSV-1 protein VP16 and its EHV-1 homologueGrapes, Matthew Giles Robert January 1999 (has links)
No description available.
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Characterisation of the HSV-1 DNA packaging protein encoded by the UL25 geneTargett-Adams, Paul January 2001 (has links)
No description available.
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An investigation into factors that influence the incorporation of proteins into the HSV-1 tegumentLeslie, Jenny January 1996 (has links)
No description available.
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Immunological control of herpes simplex virus type 1 latencyHarman, Laura Emily Rose January 2015 (has links)
No description available.
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Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infectionConn, Kristen Lea 11 1900 (has links)
Herpes simplex virus type 1 (HSV-1) genomes associate with histones in unstable nucleosomes during lytic infections. Nucleosome core particles are 146 base pairs of DNA wrapped around a histone octamer of two molecules of each H2A, H2B, H3, and H4. Histone H1 binds to nucleosomes at DNA entry and exit points. Association with histones is proposed to regulate HSV-1 gene expression. Consistently, HSV-1 transcription transactivators disrupt chromatin and HSV-1 strains mutant in these transactivators are replication impaired or transcriptionally inactive.
HSV-1 genomes have dynamic associations with histones. The genomes are not associated with histones in capsids, and input genomes are delivered to nuclear domains depleted of histones. Later during infection, HSV-1 genomes again occupy nuclear domains depleted of histones. Histone synthesis is inhibited during infection and the total level of nuclear histones remains relatively constant. It is therefore unlikely that the histones that first bind to HSV-1 genomes are newly synthesized. The source of the histones that associate with HSV-1 genomes has yet to be addressed.
Histones in cellular chromatin normally disassociate, diffuse through the nucleus, and re-associate at different sites. I propose that histones are mobilized from domains of cellular chromatin to those domains containing HSV-1 genomes in cellular attempts to silence HSV-1 gene expression. I additionally propose that HSV-1 further mobilizes histones to counteract such silencing attempts. My hypothesis is that histones are mobilized during HSV-1 infection.
In this thesis, I show that linker and core histones are mobilized during HSV-1 infection. Such mobilization results in increases to their free (not bound to chromatin) pools. Linker and core histones were mobilized even when HSV-1 proteins were not expressed, mobilization that likely reflects cellular responses to infection. Histone mobilization was enhanced when HSV-1 IE or E proteins were expressed. This enhanced mobilization was independent of HSV-1 DNA replication and late proteins. Core histones H2B and H3.3 were differentially mobilized, suggesting that different mechanisms may mobilize histones during HSV-1 infection.
My discovery of histone mobilization reveals a novel consequence of cell-virus interactions that addresses a previously unexplained aspect of HSV-1 infection.
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