Publications by authors named "Ana M Valero-Jimenez"
Article Synopsis
- Severe COVID-19 patients frequently experience coinfections with bacterial and fungal pathogens, leading to higher mortality rates compared to infections with just one pathogen.
- A study investigated blood and respiratory samples from hospitalized patients to analyze the relationship between SARS-CoV-2 and coinfections, finding no specific lineage associated with COVID-19 but noting trends in the virulence of bloodstream strains.
- Research using a mouse model demonstrated that SARS-CoV-2 infection increases susceptibility to subsequent infections with low-cytotoxicity pathogens, highlighting the enhanced risk of severe outcomes from these coinfections.
Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ferrets. Mice have the advantages of low cost, wide availability, less regulatory and husbandry challenges, and the existence of a versatile reagent and genetic toolbox. However, adult mice do not robustly transmit SARS-CoV-2.
View Article and Find Full Text PDFArticle Synopsis
- Gut microbiome dysbiosis is linked to COVID-19 severity, but a direct causal relationship has not been proven yet.
- Research shows that SARS-CoV-2 infection leads to changes in gut bacteria in mice, which could compromise gut barrier function and increase infection risk.
- Analysis of samples from 96 COVID-19 patients indicates that altered gut bacteria can enter the bloodstream, potentially causing severe secondary infections in these patients.
Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ferrets . Mice have the advantages of low cost, wide availability, less regulatory and husbandry challenges, and the existence of a versatile reagent and genetic toolbox. However, adult mice do not robustly transmit SARS-CoV-2 .
View Article and Find Full Text PDFArticle Synopsis
- * Research using a mouse model shows that SARS-CoV-2 infection disrupts the gut microbiome and affects gut cell function, mirroring findings in human patients.
- * The study found that hospitalized COVID-19 patients have an overgrowth of harmful bacteria, including antibiotic-resistant strains, which are associated with secondary infections that may originate from the gut.
Article Synopsis
- The gut microbiome has been linked to the severity of COVID-19, but a direct causal relationship had not been clearly established before this study.
- This research demonstrates that dysbiosis (imbalance) in the gut microbiome can lead to harmful bacteria entering the bloodstream during COVID-19, potentially causing serious infections.
- Analysis of stool samples from COVID-19 patients showed significant microbiome imbalances, including an increase in harmful bacteria, which aligns with findings from a mouse model that confirms viral infection adversely affects gut health.
SARS-CoV-2 and HIV are zoonotic viruses that rapidly reached pandemic scale, causing global losses and fear. The COVID-19 and AIDS pandemics ignited massive efforts worldwide to develop antiviral strategies and characterize viral architectures, biological and immunological properties, and clinical outcomes. Although both viruses have a comparable appearance as enveloped viruses with positive-stranded RNA and envelope spikes mediating cellular entry, the entry process, downstream biological and immunological pathways, clinical outcomes, and disease courses are strikingly different.
View Article and Find Full Text PDFSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of Coronavirus Disease 2019 (COVID-19). There is a dire need for novel effective antivirals to treat COVID-19, as the only approved direct-acting antiviral to date is remdesivir, targeting the viral polymerase complex. A potential alternate target in the viral life cycle is the main SARS-CoV-2 protease 3CL (M).
View Article and Find Full Text PDFSARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and an arsenal of immune antagonists. In this report, we evaluate type I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the original SARS-CoV.
View Article and Find Full Text PDFSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of Coronavirus Disease 2019 (COVID-19). There is a dire need for novel effective antivirals to treat COVID-19, as the only approved direct-acting antiviral to date is remdesivir, targeting the viral polymerase complex. A potential alternate target in the viral life cycle is the main SARS-CoV-2 protease 3CL (M).
View Article and Find Full Text PDFSARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and an arsenal of immune antagonists. In this report, we evaluate type-I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the original SARS-CoV.
View Article and Find Full Text PDFInduction of vast transcriptional programs is a central event of innate host responses to viral infections. Here we report a transcriptional program with potent antiviral activity, driven by E74-like ETS transcription factor 1 (ELF1). Using microscopy to quantify viral infection over time, we found that ELF1 inhibits eight diverse RNA and DNA viruses after multi-cycle replication.
View Article and Find Full Text PDF