Influenza A virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA743179 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability to interfere with replication-competent viruses and to induce antiviral immunity. However, the mechanisms underlying DI-mediated antiviral immunity have not been extensively explored. Here, we demonstrated interferon (IFN) independent protection conferred by influenza DI virus against homologous virus infection in mice deficient in type I and III IFN signaling. By integrating transcriptional and post-transcriptional regulatory data we identified unique host signatures in response to DI co-infection. DI-treated mice exhibited reduced viral transcription, less intense inflammatory and innate immune responses, and primed multiciliated cell differentiation in their lungs at an early stage of infection, even in the absence of type I or III IFNs. This increased multiciliogenesis could also be detected at the protein level by immunofluorescence staining of lung tissue from DI-treated mice. Overall, our study provides mechanistic insight into the protection mediated by DIs, implying a unifying theme involving inflammation and multiciliogenesis in maintaining respiratory homeostasis, and reveals their IFN-independent antiviral activity.
2023-05-15 | GSE188122 | GEO
Project description:Parasitic elements of the viral population which are unable to replicate on their own yet rise to high frequencies, defective interfering particles are found in a variety of different viruses. Their presence is associated with a loss of population fitness, both through the depletion of key cellular resources and the stimulation of innate immunity. For influenza A virus, these particles contain large internal deletions in the genomic segments which encode components of the heterotrimeric polymerase. Using a library-based approach, we comprehensively profile the growth and replication of defective species, demonstrating they possess an advantage during genome replication, and that exclusion during packaging reshapes population composition in a manner consistent with their final, observed, distribution in natural populations. We find that innate immunity is not linked to the size of a deletion; however, replication of defective segments can enhance their immunostimulatory properties. Overall, our results address several key questions in defective influenza A virus biology, and the methods we have developed to answer those questions may be broadly applied to other defective viruses.
2021-11-17 | GSE183442 | GEO
Project description:Influenza Defective Interference Particles sequencing
| PRJNA527853 | ENA
Project description:The innate immune protection provided by cationic antimicrobial peptides (CAMPs) has been shown to extend to antiviral activity, with putative mechanisms of action including direct interaction with host cells or pathogen membranes. The lack of therapeutics available for the treatment of viruses such as Venezuelan equine encephalitis virus (VEEV) underscores the urgency of novel strategies for antiviral discovery. American alligator plasma has been shown to exhibit strong in vitro antibacterial activity, and functionalized hydrogel particles have been successfully employed for the identification of specific CAMPs from alligator plasma. Here, a novel bait strategy in which particles were encapsulated in membranes from either healthy or VEEV-infected cells was implemented to identify peptides preferentially targeting infected cells for subsequent evaluation of antiviral activity. Statistical analysis of peptide identification results was used to select five candidate peptides for testing, of which three exhibited a dose-dependent inhibition of VEEV, with one peptide also significantly inhibiting infectious titers. Results suggest our bioprospecting strategy provides a versatile platform that may be adapted for antiviral peptide identification from complex biological samples.
2022-05-27 | MSV000089560 | MassIVE
Project description:Type 1 interferon (IFN) plays a critical role in early antiviral defense and priming of adaptive immunity by signalling upregulation of host antiviral interferon-stimulated genes (ISGs). Certain stimuli trigger strong activation of IFN regulatory factor 3 (IRF3) and direct upregulation of ISGs in addition to IFN. It remains unclear why some stimuli are stronger activators of IRF3 and how this leads to IFN-independent antiviral protection. We found that UV-inactivated human cytomegalovirus (HCMV) particles triggered an IFN-independent ISG signature that was absent in cells infected with UV-inactivated Sendai virus (SeV) particles. HCMV particles triggered mostly uniform activation of IRF3 and low-level IFN-? production within the population while SeV particles triggered a small fraction of cells producing abundant IFN-?. These findings suggest that population level activation of IRF3 and antiviral protection emerges from a diversity of responses occurring simultaneously in single cells. Moreover, this occurs in the absence of virus replication.
2020-05-02 | GSE149705 | GEO
Project description:Rho-associated coiled-coil kinase (ROCK) protein is a central kinase that regulates numerous cellular functions, including cellular polarity, motility, proliferation and apoptosis. Here, we demonstrate that ROCK has antiviral properties and inhibition of its activity results in enhanced propagation of human cytomegalovirus (HCMV). We show that during HCMV infection ROCK1 translocates to the nucleus and concentrates in the nucleolus were it co-localizes with the stress related chaperone, heat shock cognate 71 kDa protein (Hsc70) . Gene expression measurements showed that inhibition of ROCK activity does not affect the cellular stress response. We further demonstrate that inhibition of myosin, one of the central targets of ROCK, also increases HCMV propagation, implying that the anti-viral activity of ROCK might be mediated by activation of the actomyosin network. Finally, we demonstrate that inhibition of ROCK results in increased levels of the tegument protein UL32 and of viral DNA in the cytoplasm, suggesting ROCK activity hinders the efficient egress of HCMV particles out of the nucleus. Altogether our findings illustrate ROCK activity restricts HCMV propagation and suggest this inhibitory effect may be mediated by suppression of capsid egress out of the nucleus.
2019-07-15 | GSE134315 | GEO
Project description:The aim of this study is to phenotype a collection of 27 S. cerevisiae commercial wine strains growing within temperatures (4-45ºC) in both minimal media (SD) and synthetic must (SM) and, taking into account µmax value, to select two strains with divergent phenotype in their capacity to grow at low temperature. To confirm this differential phenotype, we design a competition between both strains during wine fermentations. As expected, at low temperature fermentation, the strain showing a good performance out-competes to the strain growing badly in cold. Finally we aimed to decipher the molecular basis underlying this divergent phenotype by analyzing the genomic, proteomic and transcriptomic differences between both strains at low temperature (15ºC) and optimum temperature (28ºC).
2015-03-31 | GSE60140 | GEO
Project description:We report a mutant that has defective pollens and abnormal anthers from its semi-sterile mutant (sstl) progeny segregates. Comparative transcriptomics analysis illustrates the mechanism of male sterility.
2019-04-15 | GSE129579 | GEO
Project description:Macrophages have important protective functions during infection with herpes simplex virus type 1 (HSV-1). However, molecular mechanisms that restrict viral propagation and protect from severe disease are unclear. Here we found that macrophages take up HSV-1 via endocytosis and transport the virions into multivesicular bodies (MVBs). In MVBs, acid ceramidase (aCDase) converts ceramide into sphingosine and increases the formation of sphingosine-rich intraluminal vesicles (ILVs). Once HSV-1 particles pass MVBs, sphingosine-rich ILVs bind to HSV-1 particles, which restricts fusion with the limiting endosomal membrane and prevents cellular infection. Lack of aCDase in macrophage cultures or in Asah1–/– mice results in replication of HSV-1 and Asah1–/– mice died soon after systemic or intravaginal inoculation. The treatment of macrophages with sphingosine enhancing compounds blocks HSV-1 propagation, suggesting a therapeutic potential of this pathway. In conclusion, we demonstrate that aCDase loads ILVs with sphingosine, which prevents HSV-1 capsids from penetrating into the cytosol.
2020-01-14 | GSE142175 | GEO