Anti-Influenza Activity of the Ribonuclease Binase in A549 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens (human)
SUBMITTER: Raihan Shah Mahmud
PROVIDER: PXD013540 | JPOST Repository | Wed Apr 17 00:00:00 BST 2019
REPOSITORIES: jPOST
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Raich_1_Kontr_RA3_01_1760.baf | Other | |||
| Raich_1_Kontr_RA3_01_1760.mgf | Mgf | |||
| Raich_1_Kontr_RA3_01_1760.mzid | Mzid | |||
| Raich_3_kl_vir_RA5_01_1764.baf | Other | |||
| Raich_3_kl_vir_RA5_01_1764.mgf | Mgf |
Items per page: 5 1 - 5 of 9 |
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Project description:Ribonucleases (RNases) of different origin demonstrate antiviral effects that are mediated by the direct RNase action on RNA species and can also involve signal transduction modulation. To reveal cellular targets and explain the mechanisms underlying the antiviral effect employed by the small extra-cellular ribonuclease of Bacillus pumilus (binase) both in vitro and in vivo, a shotgun proteomic analysis of influenza A virus (H1N1pdm09)-infected A549 cells upon binase treatment, was performed.
2019-04-18 | PXD013545 | JPOST Repository
Project description:Ribonucleases (RNases) of different origin demonstrate antiviral effects that are mediated by the direct RNase action on RNA species and can also involve signal transduction modulation. To reveal cellular targets and explain the mechanisms underlying the antiviral effect employed by the small extracellular ribonuclease of Bacillus pumilus (binase) both in vitro and in vivo, a shotgun proteomic analysis of influenza A virus (H1N1pdm09)-infected A549 cells upon binase treatment, was performed.
2019-07-29 | PXD014809 | JPOST Repository
Project description:We have previously shown that Heparin (Hep) significantly inhibited Enterovirus 71 (EV71) infection and binding in both Vero and a human neural cell line, SK-N-SH, in vitro. Therefore, in this study we intended to gain insight into the cellular and molecular mechanisms of action of Hep against clinical EV71 infection in SK-N-SH cells. Instead of stating a long list of gene functions and pathways, we tried to select for EV71-induced genes that were exclusively affected by antiviral activity of Hep through a multi-level comparison and characterization. Overall, our microarray analysis may suggest that Hep might exert its anti-EV71 activity in SK-N-SH cells, at least in part, through the following mechanisms: i. Reduction of the down-regulation effect of EV71 on TOX that would lead to an increased population of effective, mature T-cells and NK-cells; ii. Reduction of the up-regulation effect of EV71 on GIP, that in turn, would reduce recruiting different GPCRs, leading to a reduced viral infection in host cells; iii. Partially neutralization of the EV71-mediated apoptosis through expression of CARP2 that acts as an anti-apoptosis ubiquitin protein ligase (E3). EV71 is a neurovirological virus that can sometimes cause severe and fatal CNS complications in infected patients. Since still there is no approved drug for prophylaxis of EV71-casued disease, discovering a molecular drug target(s) for EV71 infection would be crucial. This was the first study to report direct assessment of mechanisms of action of antivirals against EV71 infection. SK-N-SH cells were infected with a clinical EV71 isolate followed by treatment with 125 µg/mL of Hep. At 72 hours post infection, antiviral activity and cytotoxicity of Hep at 125 µg/mL in 12-well plates were carried out at the same time as RNA extraction. This way, we could ensure that we would assess transcript profiles of the host cells under the same condition and time as assessment of antiviral activity and cytotoxicity for the same replicates. Changes in expression profiles of the host cells were comparatively assessed under four conditions: cell control (neither infection nor treatment, designated CC), treated only with Hep (compound control, designated Cyto), EV71-infected cells treated with Hep (treatment, designated H), and infected with EV71 without treatment with Hep (virus control, designated V). All experiments were applied in triplicate, and totally twelve GeneChip® Human Gene 1.0 ST arrays were purchased from Affymetrix and processed. Then, the following five contrasts were made: Hep vs. CC; VC vs. CC; Cyto vs CC; Hep vs. VC; and Hep vs. Cyto. For each contrast, only samples from the two target groups were included. The statistical parameters of ANOVAs, p values, multiple test corrections, and fold changes were calculated within each contrast. Then, a multi-level selection and analysis procedure was employed in order to attribute changes in the gene transcription level to antiviral activity of Hep.
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Project description:The recent COVID-19 pandemic shows the critical need for novel broad spectrum antiviral agents. Scorpion venoms are known to contain highly bioactive peptides, several of which have demonstrated strong antiviral activity against a range of viruses. We have generated the first annotated reference transcriptome for the Androctonus amoreuxi venom gland and used high performance liquid chromatography, transcriptome mining, circular dichroism and mass spectrometric analysis to purify and characterize twelve previously undescribed venom peptides. Selected peptides were tested for binding to the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein and inhibition of the spike RBD – human angiotensin-converting enzyme 2 (hACE2) interaction using surface plasmon resonance-based assays. Seven peptides showed dose-dependent inhibitory effects, albeit with IC50 in the high micromolar range (117–1202 μM). The most active peptide was synthesized using solid phase peptide synthesis and tested for its antiviral activity against SARS-CoV-2 (Lineage B.1.1.7). On exposure to the synthetic peptide of a human lung cell line infected with replication-competent SARS-CoV-2, we observed an IC50 of 200 nM, which was nearly 600-fold lower than that observed in the RBD – hACE2 binding inhibition assay. Our results show that scorpion venom peptides can inhibit the SARS-CoV-2 replication although unlikely through inhibition of spike RBD – hACE2 interaction as the primary mode of action. Scorpion venom peptides represent excellent scaffolds for design of novel anti-SARS-CoV-2 constrained peptides. Future studies should fully explore their antiviral mode of action as well as the structural dynamics of inhibition of target virus-host interactions.
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Project description:We have previously shown that Heparin (Hep) significantly inhibited Enterovirus 71 (EV71) infection and binding in both Vero and a human neural cell line, SK-N-SH, in vitro. Therefore, in this study we intended to gain insight into the cellular and molecular mechanisms of action of Hep against clinical EV71 infection in neural cells. Instead of stating a long list of gene functions and pathways, we tried to select for EV71-induced genes that were exclusively affected by antiviral activity of Hep through a multi-level comparison and characterization. Overall, the findings of this study suggest several molecular targets by which Hep might exert its antiviral activity against clinical EV71 infection in neural cells. Mostly, Hep appeared to modulate induction effect of EV71 on several genes in a way that may benefit the host cell and inhibit the viral infection. The most important genes where expression patterns were significantly changed by Hep include genes related to; (i) cell growth, (ii) DNA repair and replication, (iii) cytoplasmic microfilaments and related apoptosis, (iv) regulation of energy metabolism and mitochondrion-related apoptosis, (v) cytoplasmic viral transport, (vi) transmembrane proteins and the related signaling pathways, (vii) phosphoribosyltransferase, (viii) transcription factors, (ix) G protein-coupled receptors and G protein-coupled receptors-interacting proteins, (x) remodeling actin filament assembly, (xi) chemokin receptors, and (xii) immunosuppression. In addition, Hep sometimes appeared to be harmful for cells, like the case in that Hep likely suppresses regulation of Metallothionein 1E. Furthermore, it should not be ignored that the Hep-caused affects seen in this microarray analysis may partially be attributed to a significant inhibitory effect of Hep on EV71 entry into the cells. In conclusion, we propose that our microarray findings may suggest new directions for further studies on molecular targets of anti-EV71 activity of Hep. EV71 is a neurovirological virus that can cause severe and fatal CNS complications in infected patients. There is no approved drug for prophylaxis of EV71-casued disease and discovering a molecular drug target(s) for EV71 infection would be beneficial. The microarray analysis reported here was a large-scale microarray pilot study and thus further confirmatory experiments such as real time RT PCR and Western blotting would be warranted in order to confirm the mode of action of Hep implied here.
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