Publications by authors named "Nicolas Heinemann"
Inhibitors of bromodomain and extra-terminal proteins (iBETs), including JQ-1, have been suggested as potential prophylactics against SARS-CoV-2 infection. However, molecular mechanisms underlying JQ-1-mediated antiviral activity and its susceptibility to viral subversion remain incompletely understood. Pretreatment of cells with iBETs inhibited infection by SARS-CoV-2 variants and SARS-CoV, but not MERS-CoV.
View Article and Find Full Text PDFThe occurrence of immune-evasive SARS-CoV-2 strains emphasizes the importance to search for broad-acting antiviral compounds. Our previous study showed that root extract EPs 7630 has combined antiviral and immunomodulatory properties in SARS-CoV-2-infected human lung cells. Here we assessed effects of EPs 7630 in SARS-CoV-2-infected hamsters, and investigated properties of EPs 7630 and its functionally relevant constituents in context of phenotypically distinct SARS-CoV-2 variants.
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- - The study investigates the replication and cell entry characteristics of the SARS-CoV-2 variant Alpha, comparing it to the ancestral B.1 variant, and finds that Alpha spreads less efficiently than B.1 in most models.
- - Although specific genetic elements of Alpha, such as the T716I mutation, might influence its spreading abilities, its overall infectivity appears similar to B.1, with both variants showing comparable resistance to serum neutralization.
- - The research identifies a bronchial cell line (NCI-H1299) where Alpha has a significant growth advantage over B.1, and emphasizes that the variant's replication in these cells is primarily driven by its spike protein rather than ACE2 receptor expression.
Treatment options for COVID-19 are currently limited. Drugs reducing both viral loads and SARS-CoV-2-induced inflammatory responses would be ideal candidates for COVID-19 therapeutics. Previous and clinical studies suggest that the proprietary root extract EPs 7630 has antiviral and immunomodulatory properties, limiting symptom severity and disease duration of infections with several upper respiratory viruses.
View Article and Find Full Text PDFViruses manipulate cellular metabolism and macromolecule recycling processes like autophagy. Dysregulated metabolism might lead to excessive inflammatory and autoimmune responses as observed in severe and long COVID-19 patients. Here we show that SARS-CoV-2 modulates cellular metabolism and reduces autophagy.
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