Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1097360 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28589223_1.fastq.gz | Fastqsanger.gz | |||
| SRR28589223_2.fastq.gz | Fastqsanger.gz | |||
| SRR28588831_1.fastq.gz | Fastqsanger.gz | |||
| SRR28588831_2.fastq.gz | Fastqsanger.gz | |||
| SRR28582032_1.fastq.gz | Fastqsanger.gz |
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Project description:The lactococcal phage p2 is a model for studying the Skunavirus genus, the most prevalent group of phages in cheese factories worldwide. It infects L. lactis MG1363, a model strain for the study of Gram-positive bacteria. The structural proteins of phage p2 have been thoroughly described. However, most of its non-structural proteins are still uncharacterized. Here, we developed an integrative approach, making use of structural biology, genomics, physiology, and proteomics to provide insights into the function of ORF47, the most conserved non-structural protein of unknown function among the Skunavirus genus. We found this small phage protein to have a major impact on the bacterial proteome and to be important to prevent bacterial resistance to phage infection.
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Project description:Haloferax gibbonsii HFTV1 escape mutants
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Project description:Sanjuan2013 - Evolution of HIV T-cell epitope, immune activation model
Model of cellular immune response against HIV.
This model is described in the article:
Immune activation promotes evolutionary conservation of T-cell epitopes in HIV-1.
Sanjuán R, Nebot MR, Peris JB, Alcamí J.
PLoS Biol. 2013 Apr;11(4):e1001523
Abstract:
The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (TH cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when TH cell infection is concomitant to epitope recognition (trans-infection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved TH epitopes may be counterproductive.
Note from the author:
this version of the model is more general that the one described in the paper. This is because: (i) it can consider simultaneously Th-epitope escape mutants, CTL-epitope escape mutants and full T-cell (Th and CTL) escape mutants, by setting the mutation rate of Th and CTL escape mutants to zero. (ii) It allows for back mutations, which were ignored in all the simulations shown in the paper. (iii) It allows for a fitness cost of escape mutants, which was set to zero in the article. (iv) pAPCs can be infected and produce viruses (the rate of viral production for pAPCs was set to zero in the paper).
This model is hosted on BioModels Database
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by: MODEL1302180001
.
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To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2005-01-01 | MODEL1302180001 | BioModels
Project description:Purpose: To identify viral escape mutants to NA antibodies
2017-03-31 | GSE96091 | GEO
Project description:To better understand host/phage interactions and the genetic bases of phage resistance in a model system relevant to potential phage therapy, we isolated several spontaneous mutants of the USA300 S. aureus clinical isolate NRS384 that were resistant to phage K. Six of these had a single missense mutation in the host rpoC gene, which encodes the RNA polymerase beta prime subunit. To examine the hypothesis that the mutations in the host RNA polymerase affect the transcription of phage genes, we performed RNA-seq analysis on total RNA samples collected from NRS384 wild-type (WT) and rpoC G17D mutant cultures infected with phage K, at different time points after infection. Infection of the WT host led to a steady increase of phage transcription relative to the host. Our analysis allowed us to define different early, middle, and late phage genes based on their temporal expression patterns and group them into transcriptional units. Predicted promoter sequences defined by conserved -35, -10, and in some cases extended -10 elements were found upstream of early and middle genes. However, sequences upstream of late genes did not contain clear, complete, canonical promoter sequences, suggesting that factors in addition to host RNA polymerase are required for their regulated expression. Infection of the rpoC G17D mutant host led to a transcriptional pattern that was similar to the WT at early time points. However, beginning at 20 minutes after infection, transcription of late genes (such as phage structural genes and host lysis genes) was severely reduced. Our data indicate that the rpoCG17D mutation prevents the expression of phage late genes, resulting in a failed infection cycle for phage K. In addition to illuminating the global transcriptional landscape of phage K throughout the infection cycle, these studies can inform our investigations into the bases of phage K’s control of its transcriptional program as well as mechanisms of phage resistance.
2024-10-09 | GSE253516 | GEO