Oncolytic viruses have gained momentum in the last decades as a promising tool for cancer treatment. Despite the progress, only a fraction of patients show a positive response to viral therapy. One of the key variable factors contributing to therapy outcomes is interferon-dependent antiviral mechanisms in tumor cells. Here, we evaluated this factor using patient-derived glioblastoma multiforme (GBM) cultures. Cell response to the type I interferons’ (IFNs) stimulation was characterized at mRNA and protein levels. Omics analysis revealed that GBM cells overexpress interferon-stimulated genes (ISGs) and upregulate their proteins, similar to the normal cells. A conserved molecular pattern unambiguously differentiates between the preserved and defective responses. Comparing ISGs’ portraits with titration-based measurements of cell sensitivity to a panel of viruses, the “strength” of IFN-induced resistance acquired by GBM cells was ranked. The study demonstrates that suppressing a single ISG and encoding an essential antiviral protein, does not necessarily increase sensitivity to viruses. Conversely, silencing IFIT3 and PLSCR1 genes in tumor cells can negatively affect the internalization of vesicular stomatitis and Newcastle disease viruses. We present evidence of a complex relationship between the interferon response genes and other factors affecting the sensitivity of tumor cells to viruses.

Antimicrobial resistance is a serious problem in veterinary medicine worldwide. Given that farm animals are considered to be among the sources of infectious disease pathogens in humans, studying the genetic diversity of pathogenic microorganisms isolated from them and identifying strains that are potentially pathogenic to humans is a primary research task nowadays. The current paper provides a comprehensive characterization of 4 Escherichia coli strains that caused colibacillosis in farm animals. Along with a description of morphological and biochemical characteristics, data on antibiotic sensitivity are presented, and a multiple antibiotic resistance index is calculated. In order to identify the genetic basis of antimicrobial resistance (AMR), whole-genome sequencing was performed, followed by phylogenetic analysis and identification of antibiotic resistance genes. It is shown that the studied strains possess genetic determinants of virtually all major molecular mechanisms of antibiotic resistance, a significant number of which are phenotypically expressed. The pronounced potential for acquiring new variants of resistance, in combination with the strains’ virulence potential, determines the etiological significance of the E. coli isolates in relation to both farm animals and human beings. A comparison of the results obtained with other researchers’ data indicates a coincidence in the trends of the multiple antibiotic-resistant strains spread in different countries and points to the need for the development and implementation of a unified global strategy to combat AMR.