Paulo und Liang (7) (German Edition)
Contents:
Histogram of peptide ratios for all gene ontology GO -annotated proteins was quantified in experiment PM1.
The 21st Century’s 100 greatest films: Who voted?
PM only, not detected in any of experiments WCL1—3. PM annotation, plasma membrane, cell surface, extracellular, or short GO. While additional EBV genes may exist in clinical isolates, our results are consistent with the hypothesis that the majority of P3HR1 strain EBV protein-coding genes have been identified.
The Tp2 cluster included proteins important in inhibition of host innate immunity, and multiple tegument, capsid, and envelope proteins were present in the later-expressed Tp3 class. These included four of five EBV glycoproteins involved in B cell entry: Additional membrane proteins may not have been detected given their high degree of hydrophobicity, including the multipass proteins LMP1 and LMP2A. EBV establishes latency upon B cell infection. Global studies of EBV lytic reactivation have been limited by technical hurdles, such as the ability to obtain sufficient samples for systematic proteomic and viromic analysis.
Technological advances in mass spectrometry have enabled us now to provide the most complete to date temporal study of changes in the host proteome and EBV virome during lytic B cell replication. Further studies are required to identify whether soluble Ig isoforms are also targeted, and to characterize the ubiquitin-proteasome pathway by which EBV downmodulates these BCR pools.
First, a subset of lytic B cells may produce Ig reactive to antigen present on virions. BCR degradation would then enable EBV to avoid becoming trapped by binding to these antibodies within the secretory pathway or at the cell surface. Second, EBV lytic replication is thought to occur in tonsillar plasma cells, which are loaded with Igs.
Authors and titles for cs.CL in Jun 2015
Plasma cells secrete Igs at the rate of approximately 2, molecules per second Hibi and Dosch, Ig degradation may therefore shift metabolic capacity away from secretion of Ig and toward production of infectious virions, in order to prevent competition for amino acid resources. Third, multiple herpesviruses encode Ig Fc-binding proteins that enable lytic cells to evade antibody responses Hook and Friedman, Degradation of endogenous Ig may prevent an EBV-encoded Fc receptor from being fully occupied by the Fc regions of plasma cell Ig, in particular, if EBV also downregulates soluble antibody.
Additional pathways were selectively downregulated during lytic viral reactivation, including multiple components of the cell-cycle machinery. An important future goal will be to systematically compare changes in mRNA and protein abundances triggered by EBV lytic replication, in order to more fully define the extent to which EBV exerts post-transcriptional effects on host target gene expression. Multiple aspects of the EBV life cycle are intimately linked with the complement system.
We now report that EBV B cell lytic reactivation stimulates complement component production. Despite its recognized roles in host defense, complement components are increasingly implicated in regulation of metabolism and cellular survival. These observations support a model in which plasma cell differentiation provides a cue that stimulates EBV replication.
Interestingly, our findings suggest that EBV lytic replication may likewise facilitate plasma cell differentiation, through suppression of TFs that maintain germinal center state and through upregulation of factors that promote plasma cell differentiation. Thus, rather than passively activating as a bystander of plasma cell differentiation, EBV may play a more active role in remodeling the B cell environment to favor lytic replication.
To persist in an infected individual lifelong, herpesviruses have developed multiple strategies to modulate innate and adaptive immunity. One benefit is that we can use the overlap between proteins targeted by different herpesviruses to discover molecules particularly important in host defense. Clues as to viral mechanism may derive from correlation of viral and cellular protein expression patterns from our temporal analysis. Early-downregulated host proteins may be targeted by one of the earliest Tp1 or Tp2 classes of viral protein.
Innovative strategies are required to treat EBV-related diseases.
SAIT sends its finest to WorldSkills São Paulo | SAIT, Calgary, Alberta
Collectively, our studies provide a rich resource for further analyses of EBV B cell lytic replication, and herpesviral infections more widely, and identify multiple viral targets for additional analysis. Brief descriptions of key experimental procedures are provided below. For complete details, see Supplemental Experimental Procedures. FACS cells were washed twice with ice-cold PBS, followed by oxidation of sialic acid residues with sodium-meta-periodate.
Plasma-membrane glycoproteins were selectively labeled with aminooxy-biotin. The reaction was quenched, cell numbers were normalized, and then cells were lysed in Triton X Protein concentrations were determined by bicinchoninic acid assay BCA.
- SAIT sends its finest to WorldSkills São Paulo 2015.
- Girls Revenge (My Years In Middle School Book 5).
- The Path (Our Life Book 1).
Alkylated and reduced proteins were digested into peptides, which were labeled with TMT reagents, and fractions generated from combined peptide samples strong cation exchange PM samples or high pH reverse-phase high-performance liquid chromatography HPLC. Peptides were identified and quantified using a Sequest-based in-house software pipeline. Protein assembly was guided by principles of parsimony. Where all peptide spectral matches PSMs from a given EBV protein could be explained either by a canonical gene or an ORF from the six-frame translation, the canonical gene was picked in preference.
Proteins were quantified by summing TMT reporter ion counts across all matching PSM after filtering based on isolation specificity. Reverse and contaminant proteins were removed, and protein quantitation values were exported for normalization and further analysis in Excel. Further information and reagent requests may be directed to the corresponding authors. G wrote the manuscript. Supplemental Information includes Supplemental Experimental Procedures, five figures, and four tables and can be found with this article online at http: National Center for Biotechnology Information , U. Published online May Paulo , 4 Yohei Narita , 1, 6 Camille W.
Ashbaugh , 1 Chang Jiang , 1 Nicholas E. Grayson , 5 Elliott Kieff , 1, 6 Steven P. Gygi , 4 Michael P. Author information Article notes Copyright and License information Disclaimer.
This is an open access article under the CC BY license http: This article has been cited by other articles in PMC. Article plus Supplemental Information. Epstein-Barr virus, herpesvirus, lytic replication, quantitative proteomics, tandem mass tag, host-pathogen interaction, immune evasion, B cell receptor, complement, viral evasion. Open in a separate window. C Upregulated complement components, illustrated as described in B.
D Gene and protein names of all nine identified viral PM proteins. Discussion EBV establishes latency upon B cell infection. Experimental Procedures Brief descriptions of key experimental procedures are provided below.
The Act of Killing Joshua Oppenheimer, 7. Best in Show Christopher Guest, BCR degradation would then enable EBV to avoid becoming trapped by binding to these antibodies within the secretory pathway or at the cell surface. Winter Sleep Nuri Bilge Ceylan, 3. We polled critics from around the world — here is how they voted. The Social Network David Fincher, 3.
Contact for Reagent and Resource Sharing Further information and reagent requests may be directed to the corresponding authors. Footnotes Supplemental Information includes Supplemental Experimental Procedures, five figures, and four tables and can be found with this article online at http: Supplemental Information Document S1.
Click here to view. A representative term is shown from each significantly enriched cluster. Article plus Supplemental Information: An atlas of the Epstein-Barr virus transcriptome and epigenome reveals host-virus regulatory interactions. Epstein-Barr virus late gene transcription depends on the assembly of a virus-specific preinitiation complex. Detection by monoclonal antibodies of an early membrane protein induced by Epstein-Barr virus. Cytokine Growth Factor Rev.
The Epstein-Barr virus LF2 protein inhibits viral replication.
The BDLF3 gene product of Epstein-Barr virus, gp, mediates non-productive binding to heparan sulfate on epithelial cells and only the binding domain of CD21 is required for infection. Serologic markers of Epstein-Barr virus infection and nasopharyngeal carcinoma in Taiwanese men. The path from latent to productive infection. Epstein-Barr viral productive amplification reprograms nuclear architecture, DNA replication, and histone deposition. An important vaccine target for cancer prevention. Identification of new viral genes and transcript isoforms during Epstein-Barr virus reactivation using RNA-seq.
MaxQuant enables high peptide identification rates, individualized p. An Epstein-Barr virus-encoded protein complex requires an origin of lytic replication in cis to mediate late gene transcription. Effect of inhibition of viral DNA replication on their synthesis. Explore popular and recently added TV series available to stream now with Prime Video.
Start your free trial.
Find showtimes, watch trailers, browse photos, track your Watchlist and rate your favorite movies and TV shows on your phone or tablet! Keep track of everything you watch; tell your friends. Full Cast and Crew. Wait, Is Mary Poppins a Witch? Todos os filmes da minha vida. Share this Rating Title: Use the HTML below.
You must be a registered user to use the IMDb rating plugin. Photos Add Image Add an image Do you have any images for this title? Learn more More Like This. Journey to the West Letters from the South Catch a Fire Echoes of Paradise The love story between an Australian woman and a Balinese dancer.