Abstract
ABSTRACTThe heat shock response plays a role in the immune defense against viruses across various organisms. Studies on model organisms show that inducing this response prior to viral exposure enhances host resistance to infections, while deficient responses make individuals more vulnerable. Moreover, viruses rely on components of the heat shock response for their own stability and viral infections improve thermal tolerance in plants, giving infected individuals an advantage in extreme conditions, which aids the virus in replication and transmission. Here, we examine the interaction between the nematodeCaenorhabditis elegansand its natural pathogen the Orsay virus (OrV) under heat stress. We found that OrV infection leads to differential gene expression related to heat stress, and infected populations showed increased resistance to heat shock. This resistance was associated with increased expression of argonautesalg-1andalg-2, which are crucial for survival after heat shock and for OrV replication. Overall, our study suggests an environmental-dependent mutualistic relationship between the worm and OrV, potentially expanding the worm’s ecological niche and providing the virus with extra opportunities for replication and adaptation to extreme conditions.IMPORTANCEViruses have traditionally been viewed as self-serving pathogens that harm their hosts to ensure their own survival. However, recent studies are painting a different picture, revealing that viruses are ubiquitous and not always linked to diseases. In the realm of plant pathology, it has been long noted that the outcome of an infection hinges on environmental factors. Here, we show that the interaction between an animal virus and its natural host can be mutualistic under harsh temperature conditions. Our research highlights that this shift towards mutualism hinges on the expression of argonaute proteins.
Publisher
Cold Spring Harbor Laboratory