My interests in infection and immunity teaching evolved alongside 20 years of research experience related to anti-viral immunity.

Infection remains an important cause of morbidity and mortality in developed and developing countries and understanding how immune system responses to infection ensure host protection will aid us in the development of new vaccines and therapeutic innovation.

Before my switch to a teaching role, my research interests lay in characterising mechanisms that couple anti-viral immunity and cellular lipid metabolism. New and significant connections between immune pathways and sterol/ fatty acid metabolism are increasingly being described. For example, cholesterol and its metabolites have been shown to alter inflammatory mediator behavior and, conversely, immune signaling has been shown to modulate the dynamics of cholesterol transport, storage and excretion.

From a pathogen perspective, viruses are well known to alter cellular lipid metabolism to facilitate their own multiplication and, significantly, inhibition of cholesterol/fatty acid biosynthetic pathways has been shown to curtail virus replication, maturation and secretion.

It is well recognized that host interferons (IFNs), in particular IFN-α and -β, play a pivotal role in inhibiting viral growth and, in 2011, we demonstrated that interferon-mediated down-regulation of sterol biosynthesis is an integral part of the innate immune response to viral infection.

At present, the precise molecular mechanisms coupling interferon to lipid metabolism and how these mechanisms restrict viral replication remain unknown.

As a Co-PI on a BBSRC funded project focused on characterizing the mechanisms by which miRNA couple antiviral immunity to lipid metabolism, we recently uncovered a new post-transcriptional link between the immune system and cholesterol metabolism.