Sendai virus gene expression in lytically and persistently infected cells

Homann, Horst; Hofschneider, Peter Hans; Neubert, Wolfgang J.

doi:10.1016/0042-6822(90)90467-6

Cited by 37 publications

(35 citation statements)

References 36 publications

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“…The HLA class I ligands that were identified by mass spectrometry in previous studies (12,13,26) are shown in b . The transcription gradient, which was measured as the mRNA molar ratio percentage (29,34,35) ligands identified in the diverse immunoproteomics studies, respectively (Fig. 5).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, B4*0101 and B1*1301 could only bind the M 55-71 , F 91-107 , and F 199 -215 regions, and B3*0201 would be the most restrictive allele with only two possible ligands: NS1 [30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47] , and F 91-107 . As in a previous algorithm, the IEDB bioinformatics tool failed to predict the binding of all ligands that were detected by mass spectrometry to HLA-DRB3*0101.…”

Section: Theoretical Binding Affinity Of the Viral Peptides And Allelementioning

confidence: 99%

“…Only a partial correlation between this theoretical analysis and experimental detection of HLA-DR ligands (NS1 30 -47 , and F 91-107 for NetMHCIIpan and NS1 [30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47] , F 91-107, and F 199 -215 for IEDB) was found.…”

Section: Theoretical Binding Affinity Of the Viral Peptides And Allelementioning

confidence: 99%

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Structural and Nonstructural Viral Proteins Are Targets of T-Helper Immune Response against Human Respiratory Syncytial Virus

Lorente

Barriga

Barnea

et al. 2016

Molecular & Cellular Proteomics

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Newly synthesized HLA class II molecules from antigenpresenting cells associate with the class II invariant chain (Ii). These complexes are eventually transported to specialized endosomal compartments where the Ii is progressively proteolyzed until only a fragment known as the class-II-associated invariant chain peptide (CLIP) 1 remains bound in the HLA class II peptide-binding groove to prevent it from binding to cellular peptides or pathogen peptides from the endogenous pathways. Interaction of HLA class II/CLIP complexes with the accessory molecule HLA-DM induces conformational changes in HLA class II molecules. Additionally, the release of CLIP results in peptide-receptive HLA class II molecules. This compartment fuses with a late endosome that contains exogenous proteins and/or viral particles that were previously endocytosed. Thus, the binding of antigen-processed peptides of different lengths, but with specific major anchor residues that can be deeply accommodated into specific pockets of the antigen recognition site of the HLA class II molecule, produces the stabilization of the nascent HLA class II/peptide complexes and allows for their subsequent transport to the cell membrane where they are exposed for T cell recognition (1).Human respiratory syncytial virus (HRSV) (2), which is included in the Paramyxoviridae family of the Mononegavirales order, presents a single-stranded, negative-sense RNA genome that codes for 11 proteins. This enveloped pneumovirus causes repeat infections throughout life, and although in healthy adults mild infections are generally reported, the health risk in infected pediatric, immunocompromised, and elderly populations is much more serious. HRSV is the main cause of hospitalization for bronchiolitis and pneumonia in infants and young children, with infection rates approaching 70% in the first year of life (3). Worldwide, at least 3.4 million hospital admissions each year are associated with severe HRSV disease, and the global mortality rate was estimated at more than a quarter of a million deaths in 2010, mainly in developing countries (4).The immune mechanisms involved in HRSV disease and protection are not completely understood; however, it is known that infection induces mucosal and systemic humoral and cellular responses. Studies evaluating CD4 ϩ and CD8 ϩ T-lymphocyte subsets individually or together showed that both effector MHC class I-and helper MHC class II-restricted cellular responses are particularly important in clearing infections (5). Previously, some HRSV epitopes that are restricted by different HLA class II molecules were identified using T cells from seropositive individuals (6 -9). However, these experiments were performed with overlapping synthetic pepFrom the ‡Centro Nacional

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Section: Discussionmentioning

confidence: 99%

Section: Theoretical Binding Affinity Of the Viral Peptides And Allelementioning

confidence: 99%

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Structural and Nonstructural Viral Proteins Are Targets of T-Helper Immune Response against Human Respiratory Syncytial Virus

Lorente

Barriga

Barnea

et al. 2016

Molecular & Cellular Proteomics

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“…Indeed, in certain other recombinant VLP expression systems, the amounts of transfected plasmids have been adjusted to more accurately reflect or achieve cellular expression levels of the individual viral proteins produced using infectious virus (99,116,121). In an attempt to increase the amount of protein release in our system, we performed similar experimental variations in the amounts of transfected plasmids and estimated envelope glycoprotein expression in authentic NiV infection as one third of M expression and adjusted plasmid ratios accordingly (56,117,140). In additions, we further reduced the transfected amount of plasmid containing N to 50 ng per well.…”

Section: Mva Expression Of Nivmentioning

confidence: 99%

The Central Role of the Matrix Protein in Nipah Virus Assembly and Morphogenesis

Patch¹

2007

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The author hereby certifies that the use of any copyrighted material in the thesis manuscript entitled:"The Central Role of the Matrix Protein in Nipah Virus Assembly and Morphogenesis" is appropriately acknowledged and, beyond brief excerpts, is with the permission of the copyright owner. Additionally, NiV M contains a sequence that is important for budding and appears to serve as an L-domain. These findings further our understanding of paramyxovirus particle assembly in general and could help facilitate the development of a novel vaccine approach for henipaviruses.ii

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“…200,199,201 The attenuation seen with the Meredith/02 virus was therefore most similar to the measles virus. It was suggested in the case of measles that the decreased numbers of gene transcripts at the 5' end of the genome in persistently infected brain tissue could be associated with impaired budding of virus from the cell.…”

Section: Transcription Gradientmentioning

confidence: 92%

The molecular basis of the pathogenicity of Newcastle disease virus in chickens

Bergfeld¹

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Newcastle disease (ND) is a highly pathogenic disease of poultry and is caused by virulent strains of Newcastle disease virus (NDV). From 1998From -2002 there were outbreaks of ND in Australia which resulted in significant disruptions to the poultry industry. In some of these outbreaks however, the clinical signs observed in the infected birds did not appear to correlate with the World Organisation for Animal Health's definition of a virulent virus, which is based on the molecular sequence at the fusion protein cleavage site. In one particular outbreak at Meredith, Victoria, in 2002, a virulent virus was isolated, despite only a minimal increase in mortalities on the property. Therefore, this thesis has attempted to determine whether, in addition to the fusion protein cleavage site, there are other molecular determinants of pathogenicity for NDV. NDV. Sequence analysis showed a number of amino acid differences throughout the genomes of the four viruses studied, however none of these differences were in key areas such as glycosylation sites. The Meredith/02 virus was also shown to replicate well in embryonated eggs, throughout the chorioallantoic membrane and internal organs of the embryo, including the lung, liver and kidneys. This is consistent with other virulent NDVs.ii The V protein of the Meredith/02 virus was investigated for its role in potential attenuation of the virus via modulation of the host innate immune response. However there was no difference found in the ability of the Meredith/02 V protein to antagonise type I interferon in-vitro when compared with the Herts 33/56 virus.In an attempt to analyse the viral replication complex, to identify a specific protein that may be involved with the minimal pathogenicity of the Meredith/02 virus, the transcription gradient of the virus was characterized. It was found that the Meredith/02 virus has an increased transcription gradient when compared with the Herts 33/56 virus. The gradient of the Meredith/02 virus was particularly steep at the N-P junction, with particularly low levels of the P gene transcribed at 24 hours. However, gene start and end sequences at this location did not vary between the two viruses, thereby indicating that the N and P proteins are less likely to be associated with the steepened gradient. Instead, this suggests a possible role for the large polymerase protein in decreasing transcription.Whilst this research has not yet identified specific molecular sequences responsible for the minimal pathogenicity of the Meredith/02 virus despite its virulent fusion protein cleavage site, it has focused the investigation on components of the viral replication complex.Therefore directions for further research include investigating the role of the replication complex, in particular, the large polymerase (L) gene in the pathogenicity of Australian NDVs. This could also incorporate further work on the individual proteins via the use of minigenome assays, or by utilising reverse genetics and full-length virus clones.

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Sendai virus gene expression in lytically and persistently infected cells

Cited by 37 publications

References 36 publications

Structural and Nonstructural Viral Proteins Are Targets of T-Helper Immune Response against Human Respiratory Syncytial Virus

Structural and Nonstructural Viral Proteins Are Targets of T-Helper Immune Response against Human Respiratory Syncytial Virus

The Central Role of the Matrix Protein in Nipah Virus Assembly and Morphogenesis

The molecular basis of the pathogenicity of Newcastle disease virus in chickens

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