Download or read book Functional Analysis of the Transmembrane Domain and Cytoplasmic Tail of Herpes Simplex Virus Type 1 Glycoprotein H written by A. Harman and published by . This book was released on 2002 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book A Structural and Functional Analysis of Herpes Simplex Virus Type 1 Glycoprotein L an Essential Component of the Viral Fusogenic Complex written by Michael J. Novotny and published by . This book was released on 1996 with total page 456 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Biochemical and Functional Analysis of the Herpes Simplex Virus Type 1 Latency associated Transcript Promoter written by Scott Richard Millhouse and published by . This book was released on 1999 with total page 260 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Exploring the Functional Role of Herpes Simplex Virus Type 1 Glycoprotein H in Virus Entry written by Amy Yuan Zhou and published by . This book was released on 2014 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book The Role of the Cytoplasmic Domain of Herpes Simplex Virus Type 1 Glycoprotein C in Membrane Anchoring and Protein Processing written by Anne M. Skoff and published by . This book was released on 1993 with total page 216 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Functional Analysis of the Herpes Simplex Virus Type 1 Immediate early Protein ICPO written by Erik Kristian Lium and published by . This book was released on 1997 with total page 316 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Molecular and Cellular Interactions Between the Host and Herpesviruses written by and published by Frontiers Media SA. This book was released on 2021-11-09 with total page 179 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Human Herpesviruses written by Ann Arvin and published by Cambridge University Press. This book was released on 2007-08-16 with total page 1325 pages. Available in PDF, EPUB and Kindle. Book excerpt: This comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein–Barr virus, Kaposi's Sarcoma-associated herpesvirus, cytomegalovirus, HHV6A, 6B and 7, and varicella-zoster virus. The viral diseases and cancers they cause are significant and often recurrent. Their prevalence in the developed world accounts for a major burden of disease, and as a result there is a great deal of research into the pathophysiology of infection and immunobiology. Another important area covered within this volume concerns antiviral therapy and the development of vaccines. All these aspects are covered in depth, both scientifically and in terms of clinical guidelines for patient care. The text is illustrated generously throughout and is fully referenced to the latest research and developments.
Download or read book Differential Requirements for the Syncytial Phenotype of Herpes Simplex Virus Type 1 written by Akua Sarfo and published by . This book was released on 2017 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: HSV-1 encodes four glycoproteins that enable the viral membrane to fuse with the host cell, and this entry complex consists of gD (for receptor-binding), gB (the fusogen), and gH/gL (for signaling between gD and gB). Because this machinery appears on the plasma membrane of infected cells, it must be tightly regulated so that infected cells do not fuse with adjacent uninfected cells. Moreover, the fusion machinery and the proteins that regulate it are also involved in cell-to-cell spread, which enables the virus to move to uninfected cells through lateral junctions so that it can avoid neutralizing antibodies in the host. Syncytial mutants dysregulate this machinery, and cell-cell fusion results in the formation large syncytia, which contain many nuclei bounded by one membrane. Syn variants arise from mutations in any one of four HSV-1 genes, and these include gB, gK, UL20, and UL24. However, the Syn phenotype produced by these mutants is also regulated and requires accessory proteins that are involved in regulating the viral entry machinery. It has been assumed that an accessory protein required for one syn locus would be required across all the loci, and limited data support this. For example, it has been reported that accessory protein UL11 is required for both gBSyn and gKSyn. This dissertation project began with the observation that tegument protein UL21 is required for gBSyn. That is, deletion of the UL21-coding sequence from the gBSyn parent resulted in a virus that was lytic even though the syn mutation was present. Because of the assumption that accessory proteins required for one syn locus would be needed for all four, and because the UL21-coding sequence had been completely deleted, we were surprised to see syncytial variants arising from UL21/gBSyn. Similarly, passage of a virus lacking UL21 in an otherwise wild-type background also resulted in the appearance of syncytial variant viruses. We purified and sequenced these UL21 syncytial variants and found that all these mapped exclusively to glycoprotein K, a virion membrane protein capable of binding gB and thought to modulate membrane fusion events. A number of the changes we found were not gKSyn alleles described in the literature, so we followed up by creating recombinant viruses with these changes to confirm that they were indeed novel gKSyn alleles. We also confirmed that UL21 is not necessary for gKSyn-mediated fusion by building recombinant viruses with gK syncytial substitutions lacking UL21, which were immediately fusogenic following viral DNA transfection into Vero cells. Because a differential requirement for an accessory protein in syncytia formation had not been described in the literature, we tested additional gBSyn alleles for their requirement for UL21, as well as testing the requirement for UL21 in the context of UL20 and UL24 syncytial mutations. These studies revealed that UL21 is only required for gBSyn and not for any of the other syn loci. The viral proteins required for syncytia formation are thought to be similar to those needed for direct cell-to-cell spread. Herpesviruses use this spreading mechanism to avoid antibodies that could inactivate it within the infected host. To test whether UL21 is a component of the cell-to-cell spreading machinery, we examined the ability of the null virus to infect neighboring cells in the presence of neutralizing antibodies. For this, no syn mutations were present. Unlike the wild-type control, UL21 virus was found to be greatly impaired in its ability to infect adjacent cells. We hypothesize that this spreading defect provides a selective pressure for syn mutations, which compensate for the cell-to-cell spreading defect. Having identified the first example of a differential requirement for the Syn phenotype, we tested two viral proteins, gE and gI, that are well known to be required for cell-to-cell spread and the gBSyn phenotype. We tested the requirement for these two glycoproteins across the gK, UL20, and UL24Syn backgrounds. They seemed to be the logical next Syn accessory proteins to test because UL21, along with tegument proteins UL11 and UL16 forms a complex on the gE cytoplasmic tail, which is known to modulate gB function in the context of the syncytial mutation gB.A855V. We hypothesized that the requirements for gE and gI would be the same because these two proteins form a heterodimer, and based on the UL21 results, we hypothesized that neither of these glycoproteins would be required for gKSyn, UL20Syn, or UL24Syn. We were surprised to find that gE and gI are differentially required both across and within the syn loci, with UL24 syncytial mutations exhibiting a strict requirement for both gE and gI, UL20 syncytial mutations displaying a strict requirement for gE but not gI, and gK syncytial mutations displaying no requirement for gI, but an allele-specific requirement for gE. The differential requirement for gE within the gKSyn locus is the first example for an accessory protein being differentially required within one syn locus. In the course of our experiments, we also found evidence that additional syn loci might exist. This came from studies of a mutant virus that 1) lacks the UL11-binding site within the cytoplasmic tail of gE and 2) also has a gBSyn mutation (gECT(25)/gB.A855V). This virus was initially lytic when the DNA was transfected into cells; however, variants quickly arose that had the ability to fuse cells. We purified several independent variants, and confirmed that the two original mutations were present. Then, we hypothesized that the variants had gained a second syn mutation. Surprisingly, sequencing of the other three syn loci in these variants revealed no mutations. Because we could not predict what change(s) had occurred, a whole-genome, deep sequencing approach was used. The results revealed that all had mutations that prevented the expression of glycoprotein C, a viral protein implicated in adsorption of the virus to cells but also described in the literature as decidedly not a syn locus. This provides the first evidence that gC regulates the fusion activity of gB.
Download or read book Cumulated Index Medicus written by and published by . This book was released on 1997 with total page 1860 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Virus Entry written by Thomas Mettenleiter and published by Academic Press. This book was released on 2019-08-16 with total page 358 pages. Available in PDF, EPUB and Kindle. Book excerpt: Virus Entry, Volume 104, the latest release in the Advances in Virus Research series, highlights new advances in the field, with this new volume presenting interesting chapters on plant virus cell-to-cell entry, plant virus entry via insect transmission, VSV/Rabies virus entry, Papovavirus entry, New approaches to study fusion proteins, Hantavirus receptors, Gamma Herpesvirus entry, and many other interesting topics. - Provides the authority and expertise of leading contributors from an international board of authors - Presents the latest release in the Advances in Virus Research series - Includes the latest information on virus structure and function
Download or read book Contributions of Amphipathic Helices and the Cytoplasmic Tail of the Herpes Simplex Virus Type 2 Glycoprotein B to Its Role in Membrane Fusion written by Daniel David Norton and published by . This book was released on 2000 with total page 342 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Studies on the Function and Antigenicity of Glycoprotein H of Herpes Simplex Virus Type 1 written by Audrey Jane Forrester and published by . This book was released on 1991 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Functional Analysis of the A Sequence of Herpes Simplex Virus 1 written by Joany Chou and published by . This book was released on 1986 with total page 278 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Structural and Functional Analysis of Herpes Simplex Virus Type 2 Glycoprotein B written by Huiling Chiou and published by . This book was released on 1991 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Glycoprotein M and ESCRT in Herpes Simplex Virus Type 1 Assembly written by Yudan Ren and published by . This book was released on 2012 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Herpes simplex virus type 1 (HSV-1) has a large linear double-stranded DNA genome in an icosahedral capsid shell, a cell-derived lipid envelope and a proteinaceous tegument layer. There are over fifty viral proteins and many host proteins identified in HSV-1 virions. The final formation of mature virus particles requires the membrane wrapping of tegumented capsids in the cytoplasm, a process termed secondary envelopment. This process involves the coordination of numerous viral and cellular proteins and results in double-membrane structures with enveloped virions contained within cellular vesicles. Mature viruses are then released through the fusion of these virion-containing vesicles and plasma membranes. This thesis describes investigation into the functions of viral glycoprotein M (gM) and the cellular Endosomal Sorting Complexes Required for Transport (ESCRT) in secondary envelopment. Firstly, it has been reported that gH/L can be efficiently internalised and targeted to the TGN by the co-expression of gM in transfection assays. In order to examine the role of gM in guiding the localisation of viral proteins in infected cells, a HSV-1 gM deletion virus (∆gM), and its revertant virus were constructed. The major phenotype demonstrated was that the absence of gM caused the internalisation of cell surface gH/L to be inhibited and higher levels of gH/L to be observed on the cell surface. Further, lower levels of gH/L were detected in purified ∆gM virions, which was in agreement with the delayed entry kinetics, smaller plaque sizes and greater replication deficits at low multiplicity of infection observed in ∆gM infected cells. Over all the results presented in this thesis demonstrate that in infected cells the efficient incorporation of gH/L into virions relies on the function of gM in HSV-1. Secondly, during HSV-1 secondary envelopment the budding and scission of the viral envelope from the host membrane share topological similarities with the formation of intraluminal vesicle in multivesicular bodies, retrovirus budding, and abscission at the end of cytokinesis, processes that require the cellular ESCRT machinery. There are four multiprotein ESCRT complexes and many associated proteins involved in their regulation. It has been previously shown that the ESCRT-III complex and a functional ATPase VPS4 are required for HSV-1 secondary envelopment, but different from the strategy utilised by HIV-1, the recruitment of ESCRT during HSV-1 infection is independent of TSG101 and/or ALIX. Data presented in this thesis demonstrate that CHMP4A/B/C proteins of the ESCRT-III complex are specifically crucial for HSV-1 secondary envelopment. Simultaneous depletion of CHMP4A/B/C proteins significantly inhibited HSV-1 replication. Ultrastructure analysis revealed that there were virtually no extracellular virions in CHMP4A/B/C depleted samples while more free capsids were observed in the cytoplasm, although the nuclear capsids and primary envelopment events appeared to be normal. In order to identify interactions between HSV-1 and ESCRT proteins, 22 HSV-1 tegument proteins were cloned and tested against a panel of ESCRT and ESCRT-associated proteins in yeast two-hydrid assays. Analysis of positive hits from yeast two-hybrid interaction screens using GST pull-down, co-immunoprecipitation and protein co-localisation assays have validated interactions of pUL47 with CC2D1A/1B, CIN85, CHMP6 and ALIX, pUL46 and pUL49 with CC2D1A/1B and CIN85, and pUL16 with CC2D1A/1B. Furthermore, the newly identified ESCRT associated proteins CC2D1A and CC2D1B have been detected in purified virions. The role of the identified ESCRT proteins in HSV-1 replication has been investigated using siRNA depletion. Unfortunately siRNA depletions of the various ESCRT candidates individually or in combinations did not show any significant effect on HSV-1 replication. Overall these data suggest that unlike HIV and other retroviruses, HSV-1 has evolved multiple parallel pathways to hijack the ESCRT machinery to facilitate its replication, particularly, through the interactions that lead directly to the recruitment of CHMP4A/B/C proteins. Disruption of some of these pathways did not prevent HSV-1 replication in tissue culture, suggesting any one potential pathway is sufficient for ESCRT recruitment to sites of HSV-1 assembly.
Download or read book Functional Analysis of Two Early Gene Promoters of Herpes Simplex Virus Type 1 written by Nupur T. Pande and published by . This book was released on 1997 with total page 352 pages. Available in PDF, EPUB and Kindle. Book excerpt:
