Publications by authors named "M Schmolke"
Introduction: Respiratory viral infections (RVIs) are a major global contributor to morbidity and mortality. The susceptibility and outcome of RVIs are strongly age-dependent and show considerable inter-population differences, pointing to genetically and/or environmentally driven developmental variability. The factors determining the age-dependency and shaping the age-related changes of human anti-RVI immunity after birth are still elusive.
View Article and Find Full Text PDFThe WHO declared the official end of the SARS-CoV-2 caused public health emergency on May 5th, 2023, after two years in which the virus infected approximately 750 Mio individuals causing estimated up to 7 Mio deaths. Likely, the virus will continue to evolve in the human population as a seasonal respiratory pathogen. To now prevent severe infection outcomes in vulnerable individuals, effective antivirals are urgently needed to complement the protection provided by vaccines.
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- Influenza A virus infection activates the NLRP3 inflammasome, leading to the release of the proinflammatory cytokine IL-1β from immune cells, which contributes to inflammation and fever.
- The contemporary PB1-F2 protein from certain IAV strains inhibits NLRP3 activation via a specific four-amino acid motif (TQGS) that affects the binding and localization of PB1-F2.
- Phylogenetic analysis indicates that this NLRP3 inhibitory motif is conserved across recent human-infecting IAV strains, providing insight into the molecular mechanisms of immune evasion by the virus.
For virus infection of new host cells, the disassembly of the protective outer protein shell (capsid) is a critical step, but the mechanisms and host-virus interactions underlying the dynamic, active, and regulated uncoating process are largely unknown. Here, we develop an experimentally supported, multiscale kinetics model that elucidates mechanisms of influenza A virus (IAV) uncoating in cells. Biophysical modeling demonstrates that interactions between capsid M1 proteins, host histone deacetylase 6 (HDAC6), and molecular motors can physically break the capsid in a tug-of-war mechanism.
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- Influenza virus infection impacts both lung and gut bacteria, but most studies only look at the composition of these microbiota.
- During influenza A virus (IAV) infection, the gut microbiome decreases and loses the ability to metabolize certain nutrients in oxygen-rich environments.
- There is also an increase in resistance to important antibiotics, which could complicate treatment strategies for infections involving multiple bacteria.