Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA287112 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2064020.fastq.gz | Fastqsanger.gz | |||
| SRR2064030.fastq.gz | Fastqsanger.gz | |||
| SRR2064021.fastq.gz | Fastqsanger.gz | |||
| SRR2064022.fastq.gz | Fastqsanger.gz | |||
| SRR2064023.fastq.gz | Fastqsanger.gz |
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Project description:The complex life cycle of herpesviruses is orchestrated by the interplay of host factors and hundreds of viral genes. Understanding how they work together and how perturbations of viral and host factors impact infection represents both a fundamental problem in virology and the basis for designing antiviral interventions. Here, we use CRISPR screening to study infection of human cytomegalovirus (HCMV) in primary cells, comprehensively defining the functional contribution of each viral and host factor. We then record the transcriptomes of tens of thousands of single cells, and monitor how genetic perturbation of critical host and viral factors alters the timing, course, and progression of infection. We find that normally, the large majority of cells follow a stereotypical transcriptional trajectory. Perturbing critical host factors does not change this trajectory per se, but can either stall, delay or accelerate progression along the trajectory, allowing us to pinpoint systematically the stage of infection at which each host factor acts. Conversely, perturbation of viral factors can create distinct abortive trajectories. Our results reveal a dichotomy between the roles of host and viral factors and more generally provide a road map for functional dissection of host-pathogen interactions.
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Project description:Genetic screens have transformed our ability to interrogate cellular factor requirements in infection, yet current approaches are limited in their sensitivity, biased towards early stages of infection and provide only simplistic phenotypic information which is often based on infected cell survival. Here, by engineering human cytomegalovirus to express sgRNA libraries directly from the viral genome, we developed a sensitive, versatile, viral centric approach that allows profiling of different stages along viral infection in a pooled format. Using this approach, which we termed VECOS (Virus Encoded CRISPR-based direct readOut Screening system), we identified hundreds of novel dependency and restriction factors and we quantified their direct effects on viral genome replication, viral particle secretion and infectiousness of secreted particles, providing a multi-dimensional perspective on viral-host interactions. These high resolution measurements reveal that perturbations that alter late stages in HCMV life cycle mostly regulate HCMV particle quality rather than quantity, defining correct virion assembly as a critical stage that is heavily reliant on viral-host interactions. Overall, VECOS facilitates systematic high resolution dissection of human proteins' role along the infection cycle, providing a roadmap for in-depth dissection of host–herpesvirus interactions.
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2017-03-31 | MSV000080853 | MassIVE
Project description:Human cytomegalovirus (HCMV) is an important pathogen that extensively modulates host cells, downregulating >900 human proteins over the course of viral replication and degrading ≥133 proteins shortly after infection. The mechanism of degradation of most host proteins remains unresolved, and the functions of many viral proteins are incompletely characterised. We performed a systematic interactome analysis of 169 canonical HCMV proteins, and a subset of non-canonical HCMV proteins, in infected cells. This identified an extensive network of >3,400 virus-host and >150 virus-virus protein interactions, providing insights into novel functions for multiple viral genes. Domain analysis predicted binding of the viral UL25 protein to the SH3 domains of NCK Adaptor Protein 1. Viral interacting proteins were identified for 31/133 degraded host targets. Finally, the uncharacterised, non-canonical ORFL147C protein was found to interact with elements of the mRNA splicing machinery, and a mutational study suggested its importance in viral replication. The interactome data will be important for future studies of herpesvirus infection.
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Project description:The interplay between pathogens and hosts has been studied for decades using targeted approaches such as the analysis of mutants and host immunological responses. Although much has been learned from such studies, they focus on individual pathways and fail to reveal the global effects of infection on the host. To alleviate this issue, high-throughput methods such as transcriptomics and proteomics have been used to study host-pathogen interactions. Recently, metabolomics was established as a new method to study changes in the biochemical composition of host tissues. We report a metabolomics study of Salmonella enterica serovar Typhimurium infection. We used Fourier Transform Ion Cyclotron Resonance Mass Spectrometry with Direct Infusion to reveal that dozens of host metabolic pathways are affected by Salmonella in a murine infection model. In particular, multiple host hormone pathways are disrupted. Our results identify unappreciated effects of infection on host metabolism and shed light on mechanisms used by Salmonella to cause disease, and by the host to counter infection.
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Project description:Arabidopsis ecotype Col-0 expressing RPL18 fused to His & Flag epitopes (RPL18-HF) under 35S control was used to discern the effects of Turnip mosaic virus (TuMV) infection on host translation initiation. Plants were grown in LC-1 soil in 12 hour days and infected by TuMV-GFP or mock-inoculated just prior to sending up bolts. Samples were taken from rosette leaves 10 days after inoculation. Only tissue fluorescing GFP was selected from the virus-infected samples. Similar tissue was sampled from mock-infected leaves. FLAG antibody was used to isolate RPL18-HF. The RNA co-immunoprecipitated with RPL18-HF is fully translation-initiated. This translation-initiated RNA, also referred to as polysomal RNA, was isolated and compared to total RNA under both mock and TuMV-infected states to find TuMV-induced changes in host translation initiation. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Jackson Moeller. The equivalent experiment is AT42 at PLEXdb.] pathogen infection: TuMV inoculated - RNA fraction: polysomal RNA(3-replications); pathogen infection: TuMV inoculated - RNA fraction: total RNA(3-replications); pathogen infection: mock inoculated - RNA fraction: polysomal RNA(3-replications); pathogen infection: mock inoculated - RNA fraction: total RNA(3-replications)
2011-03-11 | E-GEOD-20278 | biostudies-arrayexpress
Project description:The goal of this experiment was to examine the effects of Blumeria gramins f. sp. hordei (Bgh) on the host process of translation initiation in both incompatible and compatible interactions with Hordeum vulgare. This was done by using Bgh isolate 5874 (AVRa6) on the resistant host CI 16151 (Mla6) and fast-neutron derived, loss-of-function mutant m9472 (mla6). Plants were grown 7 days in the greenhouse and then inoculated or non-inoculated and transferred to an 18°C growth chamber with an 8 hr dark, 16 hr light photoperiod. At 32 hours after infection the tissue was harvested and immediately frozen in liquid nitrogen. From the same tissue, total RNA was isolated using a Trizol method, while polysomal RNA was isolated by sucrose density centrifugation. Three biological replications were conducted. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Jackson Moeller. The equivalent experiment is BB72 at PLEXdb.] genotype:CI 16151 (Mla6)-pathogen infection: Bgh isolate 5874 (AVRa6)-RNA fraction:polysomal RNA(3-reps); genotype:CI 16151 (Mla6)-pathogen infection: Bgh isolate 5874 (AVRa6)-RNA fraction:total RNA(3-reps); genotype:CI 16151 (Mla6)-pathogen infection:non-inoculated-RNA fraction:polysomal RNA(3-reps); genotype:CI 16151 (Mla6)-pathogen infection:non-inoculated-RNA fraction:total RNA(3-reps); genotype:CI 16151 m9472 (mla6)-pathogen infection: Bgh isolate 5874 (AVRa6)-RNA fraction:polysomal RNA(3-reps); genotype:CI 16151 m9472 (mla6)-pathogen infection: Bgh isolate 5874 (AVRa6)-RNA fraction:total RNA(3-reps); genotype:CI 16151 m9472 (mla6)-pathogen infection:non-inoculated-RNA fraction:polysomal RNA(3-reps); genotype:CI 16151 m9472 (mla6)-pathogen infection:non-inoculated-RNA fraction:total RNA(3-reps)
2011-03-11 | E-GEOD-20279 | biostudies-arrayexpress