Similar Datasets
Project description:SARS-CoV-2 can generate viral microRNAs (v-miRNAs) that target host gene expression. This study used small RNAseq to identify the v-miRNAs present in COVID-19 patients' nasopharyngeal swabs. The study identified a specific conserved v-miRNA sequence (CoV2-miR-O8) unique to SARS-CoV-2 that is highly present in COVID-19 patients' samples, interacts with Argonaute, and has features consistent with Dicer and Drosha generation. CoV2-miR-O8 is predicted to target specific human genes and can be detected by RTPCR assays in patients.
2023-12-11 | GSE230080 | GEO
Project description:Endothelial cell infection and dysfunction, immune activation in severe COVID-19
| PRJNA734526 | ENA
Project description:The coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains to spread worldwide. COVID-19 is characterized by the striking high mortality in elderly; however, its mechanistic insights remain unclear. Systemic thrombosis has been highlighted in the pathogenesis of COVID-19, and lung microangiopathy in association with endothelial cells (ECs) injury has been reported by post-mortem analysis of the lungs. Here, we experimentally investigated the SARS-CoV-2 infection in cultured human ECs, and performed a comparative analysis for post-infection molecular events using early passage and replicative senescent ECs. We found that; 1) SARS-CoV-2 infects ECs but does not replicate and disappears in 72 hours without causing severe cell damage, 2) Senescent ECs are highly susceptible to SARS-CoV-2 infection, 3) SARS-CoV-2 infection alters various genes expression, which could cause EC dysfunctions, 4) More genes expression is affected in senescent ECs by SARS-CoV-2 infection than in early passage ECs, which might causes further exacerbated dysfunction in senescent ECs. These data suggest that sustained EC dysfunctions due to SARS-CoV-2 infection may contribute to the microangiopathy in the lungs, leading to deteriorated inflammation and thrombosis in COVID-19. Our data also suggest a possible causative role of EC senescence in the aggravated disease in elder COVID-19 patients.
2023-05-01 | GSE206677 | GEO
Project description: Not available
| S-EPMC8315069 | biostudies-literature
Project description:SARS-CoV-2 infection may result in a severe pneumonia associated to elevation of blood inflammatory parameters, reminiscent of cytokine storm syndrome. Steroidal anti-inflammatory therapies have shown efficacy in reducing mortality in critically ill patients, however the mechanisms by which SARS-CoV2 virus trigger such an extensive inflammation remain unexplained. A pivotal cytokine driving inflammatory phenotypes is IL-1β, whose maturation and secretion is regulated by NLRP3 inflammasome. In the present report we provide a mechanistic explanation for the strong inflammatory manifestations associated to COVID-19 and further evidence that NLRP3 and IL-1β targeting could be an effective strategy in this disease.
2022-12-23 | GSE163317 | GEO
Project description:Genomic surveillance of SARS-CoV2 in Argentina
| PRJEB46220 | ENA
Project description:Obesity is a risk factor for developing severe COVID-19. However, the mechanism underlying obesity-accelerated COVID-19 remains unclear. Here, we report results from a study in which K18-hACE2 mice were fed an obesity-inducing western diet (WD) for over 3 months before intranasal infection with SARS-CoV2. After infection, the WD-fed K18-hACE2 mice lost more body weight and had more severe lung inflammation than normal chow (NC)-fed mice. Bulk RNAseq analysis of lungs and adipose tissue revealed that a diverse landscape of various immune cells, inflammatory markers, and pathways are upregulated in obese COVID-19 patients or the WD-fed K18-hACE2 mice when compared with their respective control groups. When compared with infected NC-fed mice in the lung, the infected WD-fed mice had upregulation of IL-6, a well-established marker for severe COVID-19. These results indicate that obesity-accelerated severe COVID-19 caused by SARS-CoV-2 infection in the K18-hACE2 mouse model can be used for dissecting the cellular and molecular mechanisms underlying pathogenesis. Furthermore, in the transcriptome analysis of the lung and adipose tissue obtained from deceased COVID-19 patients, we found upregulation of an array of genes and pathways associated with Inflammation. Both the K18-hACE2 mouse model and human COVID-19 patient data support a link between inflammation and an obesity-accelerated COVID-19 disease phenotype.
2024-05-21 | GSE267021 | GEO
Project description:The ongoing pandemic of coronavirus disease 2019 (COVID-19), which results from the rapid spread of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a significant global public health threat, with molecular mechanisms underlying its pathogenesis largely unknown. Small non-coding RNAs (sncRNAs) are known to play important roles in almost all biological processes. In the context of viral infections, sncRNAs have been shown to regulate the host responses, viral replication, and host-virus interaction. Compared with other subfamilies of sncRNAs, including microRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs), tRNA-derived RNA fragments (tRFs) are relatively new and emerge as a significant regulator of host-virus interactions. Using T4 PNK‐RNA‐seq, a modified next‐generation sequencing (NGS), we recently found that nasopharyngeal swabs (NPS) samples from SARS-CoV-2 positive and negative subjects show a significant difference in sncRNA profiles. There are about 166 SARS-CoV- 2-impacted sncRNAs. Among them, tRFs are the most significantly affected and almost all impacted tRFs are derived from the 5’-end of tRNAs (tRF5). Using a modified qRT-PCR, which was recently developed to specifically quantify tRF5s by isolating the tRF signals from its corresponding parent tRNA signals, we validated that tRF5s derived from tRNA GluCTC (tRF5-GluCTC), LysCTT (tRF5-LysCTT), ValCAC (tRF5-ValCAC), CysGCA (tRF5-CysGCA) and GlnCTG (tRF5-GlnCTG) are enhanced in NPS samples of SARS-CoV2 patients and SARS-CoV2-infected airway epithelial cells. In addition to host-derived ncRNAs, we also identified several sncRNAs derived from the virus (svRNAs), among which a svRNA derived from CoV2 genomic site 346 to 382 (sv-CoV2-346) has the highest expression. The induction of both tRFs and sv-CoV2-346 has not been reported previously, as the lack of the 3’-OH ends of these sncRNAs prevents them to be detected by routine NGS. In summary, our studies demonstrated the involvement of tRFs in COVID-19 and revealed new CoV2 svRNAs.
2022-03-01 | GSE193555 | GEO
Project description:Describe the transcriptomic profile of Golden Hamster olfactory bulb in response to SARS-CoV-2 infection, separating by sexes.
2021-06-19 | E-MTAB-10442 | biostudies-arrayexpress