The various stages of viral entry, replication, assembly, and secretion have specific environmental requirements. Efficient viral propagation requires therefore that viruses remodel their host cell. This is accomplished via modulation of host cell pathways and signalling systems, which alter the metabolic profile of the cell. The immunometabolic response to infection, part of the innate immune response, aims to reverse these alterations by targeting the same pathways. 

A primary area of focus for our group is deciphering the roles of non-coding RNAs, including miRNAs and long non-coding RNAs, in the context of host-pathogen interactions. miRNAs are short, non-coding strands of RNA which play important roles in modulating gene expression through interactions with host or viral miRNAs, thereby regulating numerous cell pathways. This regulatory mechanism is targeted by pathogens in order to establish a cellular environment suitable for a productive infection. Work in our group has demonstrated that viruses are able to hijack host miRNAs involved in regulation of metabolic and immune-related pathways to promote pathogenesis. We have also identified mechanisms through which the host uses miRNAs to restrict the pathogen life cycle. 

​Remodelling of the host cell is carried out and regulated by host cell enzymes. miRNAs can affect this remodelling by directly targeting and reducing the expression of an enzymes of interest, or by targeting their up-stream regulators. Identifying host enzymes directly or indirectly regulated by miRNAs, viruses, and the immune response provides a better understanding of the pivotal role miRNAs play in the arms-race between viral propagation and the immunometabolic response.

For more details, see our microRNAs in host-pathogen interactions page.