Friedemann Weber

This paper identifies eIF4A as a druggable host factor in insect vectors that can be targeted by rocaglates and pateamines to suppress arboviral replication.

This study identifies MED13 and DDX60 as critical host factors for SARS-CoV-2 infection through a haploid genetic screen in mouse cells.

This study recovers an ancient Bandavirus genome from a 1919 bat sample and identifies its modern presence in European bats, showing its ability to block interferon induction.

This paper investigates the cell line tropism, interferon system interactions, and NSs mechanisms of Ntepes and Gabek Forest phleboviruses, finding they can infect human cell lines and inhibit the interferon system similar to Rift Valley fever virus.

This study shows JAK inhibitors like baricitinib suppress IFN-stimulated genes, aiding viral propagation by reducing antiviral defenses.

This study identifies SFSV NSs as a viral protein that suppresses the integrated stress response by binding to eIF2B and preventing eIF2(P) from inhibiting nucleotide exchange.

This study shows that defective interfering particles (DIPs) primarily exert antiviral activity through interferon (IFN) system activation rather than suppression of viral replication.

This study maps the RNA-RNA interactome of SARS-CoV-2, revealing long-range interactions and conserved structural elements important for viral replication and translation.

The paper annotates and analyzes non-coding RNAs in 16 bat genomes, revealing new expression patterns and providing a resource for studying bat biology and host-virus interactions.