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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The effects on Langerhans cells and dermal leukocyte populations of agents which trigger herpes simplex reactivation

Manickasingham, Shrivanthi Prithiva January 1996 (has links)
No description available.
2

The role of Langerhans cells in infection with herpes simplex virus

Williams, N. A. January 1989 (has links)
No description available.
3

Analysis of transcriptional activation by the HSV-1 protein VP16 and its EHV-1 homologue

Grapes, Matthew Giles Robert January 1999 (has links)
No description available.
4

Characterisation of the HSV-1 DNA packaging protein encoded by the UL25 gene

Targett-Adams, Paul January 2001 (has links)
No description available.
5

An investigation into factors that influence the incorporation of proteins into the HSV-1 tegument

Leslie, Jenny January 1996 (has links)
No description available.
6

Immunological control of herpes simplex virus type 1 latency

Harman, Laura Emily Rose January 2015 (has links)
No description available.
7

Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection

Conn, 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.
8

Inhibition of PACT mediated type 1 interferon production by herpes simplex virus type 1 Us11 protein

Kew, Chun, 喬駿 January 2014 (has links)
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
9

Studies on the role of the cellular ESCRT machinery in herpes simplex virus type 1 replication

Pawliczek, Tobias January 2011 (has links)
No description available.
10

Study of herpes simplex virus type 1 tegument assembly

Svobodová, Stanislava January 2013 (has links)
No description available.

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