https://www.selleckchem.com/products/bai1.html Knowledge on bornaviruses has expanded tremendously during the last decade through detection of novel bornaviruses and endogenous bornavirus-like elements in many eukaryote genomes, as well as by confirmation of insectivores as reservoir species for classical Borna disease virus 1 (BoDV-1). The most intriguing finding was the demonstration of the zoonotic potential of lethal human bornavirus infections caused by a novel bornavirus of different squirrel species (variegated squirrel 1 bornavirus, VSBV-1) and by BoDV-1 known as the causative agent for the classical Borna disease in horses and sheep. Whereas a T cell-mediated immunopathology has already been confirmed as key disease mechanism for infection with BoDV-1 by experimental studies in rodents, the underlying pathomechanisms remain less clear for human bornavirus infections, infection with other bornaviruses or infection of reservoir species. Thus, an overview of current knowledge on the pathogenesis of bornavirus infections focusing on immunopathology is given.Positive-strand RNA viruses need to arrogate many cellular resources to support their replication and infection cycles. These viruses co-opt host factors, lipids and subcellular membranes and exploit cellular metabolites to built viral replication organelles in infected cells. However, the host cells have their defensive arsenal of factors to protect themselves from easy exploitation by viruses. In this review, the author discusses an emerging arms race for cellular resources between viruses and hosts, which occur during the early events of virus-host interactions. Recent findings with tomato bushy stunt virus and its hosts revealed that the need of the virus to exploit and co-opt given members of protein families provides an opportunity for the host to deploy additional members of the same or associated protein family to interfere with virus replication. Three examples with well-established heat shock prote