Ontology highlight
ABSTRACT:
PROVIDER: PRJNA942601 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Grouper is an important commercial maricultural fish, which suffer viral nervous necrosis (VNN) disease at the larval and juvenile stages, but the changes of transcriptomics and proteomics during viral infection remain unknown. In this study, we applied RNA-seq and label-free mass spectrum for the first time to depict the map of transcriptomics and proteomics in non-infected, susceptible-infected and tolerate-infected grouper in larval stage. Further analyses showed that the transcriptome and proteome change dramatically among 3 distinct groups, indicating that different immune response for infected and perststent grouper in larval stage. These valuable transcriptomics and proteomics datasets enable the investigation of molecular mechanism in nervous necrosis (VNN) virus infection, thus helps the further development of molecular breeding and marine fishery
2019-05-15 | PXD012763 | Pride
Project description:Purpose:To study the molecular mechanism of nerve necrosis (VNN) virus infection, and to provide help for molecular breeding and further development of Marine fishery Results: we found that 17,939 genes are elevated after NNV infection compared with control group, suggesting that NNV infection can strongly induce the expression of immune associated genes. In summary, we obtained high quality transcriptome of orange-spotted grouper and comparative analysis of transcriptome analysis reveals dramatically perturbation of gene expression with NNV infection.
2020-02-14 | GSE126620 | GEO
Project description:Next generation sequencing facilitates quantitative analysis of control samples and nervous necrosis (VNN) virus infection samples orange-spotted grouper transcriptomes
| PRJNA522739 | ENA
Project description:The goal of this study was to determine how an HIV quasispecies is maintained in the face of selection. We deep sequenced the HIV provirus from cell populations as well as single cells at different time points from in vitro evolution experiments and found that when a less fit and more fit infect the same cell, they share components (complmentation) and therefore allow the less fit to perpetuate. We reproduced a quasispecies to an HIV reverse transcriptase inhibitor. The drug resistant genotype never completely supplanted the drug sensitive genotype, which stabilized at about 20% of viral sequences. Single-cell sequencing showed that resistant genotype frequency plateaued when cells were co-infected with sensitive and resistant genotypes, suggesting a sharing of viral proteins in co-infected cells (complementation), masking genotypic differences. To test if complementation can confer phenotypic drug resistance, we co-transfected fluorescently labelled molecular clones of sensitive and resistant HIV and observed drug resistance in genotypically sensitive virus from co-transfected cells. Resistant virus preferentially co-infected cells with drug sensitive HIV, explaining initiation of co-infections. Modelling showed that a stable quasispecies could form at the experimental multiplicities of infection. Conclusions: Complementation can lead to a quasispecies in infection environments where multiple infections per cell are common
2020-05-13 | GSE150390 | GEO
Project description:The biological basis for the increased severity of influenza A viruses during the 2009 influenza pandemic remains unclear. Intra-host evolution of quasispecies and strong inflammation were identified as important hallmarks of severe pandemic H1N1 influenza A virus 2009 (A(H1N1)pdm09) infection. HA-222D/G quasispecies of A(H1N1)pdm09 were shown to undergo fast evolution and to cause severe influenza in human and mice. Here, we analysed the whole genome transcriptional response of mice infected with the A/Jena/5258/09 (mpJena/5258) virus over a period of 12 days to gain insights into the pathogenesis of A(H1N1)pdm09 HA-222D/G quasispecies on a molecular level. Remarkably, the transcriptional response to severe mpJena/5258 showed biphasic expression profile for the majority of genes which was never shown before. The gene expression analysis shows first peak with 968 differentially expressed genes at day 2 post infection (p.i.), followed by a stagnant recovery phase with 359 differentially expressed genes at day 4 p.i., and a second peak with 1001 differentially expressed genes at day 7 p.i., finally followed by a recovery phase. Using a reverse engineering strategy, a regulatory network was inferred to identify key interactions leading to severe pathogenesis of mpJena/5258. Known regulatory interactions were extracted by Pathway Studio 9.0 and softly integrated during network inference. The results demonstrate a hyper-responsive action and a positive feedback loop of IFN gamma (Ifng), Stat1 and Tlr3 signalling during mpJena/5258 infection. In conclusion, mpJena/5258 infection is associated with biphasic gene expression profile and a positive feedback mechanism of Ifng which correlates with the evolution of HA-222D/G quasispecies and leads to overwhelming immune response. A significant correlation were found between the co-expression action of three genes (Ifng, Stat1 and Tlr3) with a phenomenological clinical symptom score.
2017-02-10 | GSE67241 | GEO
Project description:DLB-1 cell line were mock infected or infected with nervous necrosis virus (NNV).
2018-12-13 | GSE118060 | GEO