Ana Traven obtained her PhD in 2002 from the University of Zagreb Croatia. As a postdoctoral fellow, she trained at the St. Vincent’s Institute in Melbourne (supported by the NHMRC Peter Doherty training fellowship), and in the Department of Microbiology at Columbia University in New York City (supported by a Short-Term Postdoctoral Fellowship from the Human Frontier Science Program Organisation). In 2009 Ana started her own research group at Monash University, where she is currently an Associate Professor and Head of the Laboratory for fungal pathogenesis.

As a PhD student and postdoctoral fellow, Ana used the yeast Saccharomyces cerevisiae as a model system to understand gene regulation. More recently, her research moved into the field of human fungal pathogens, focusing on the yeast Candida albicans. Potentially deadly infections with Candida threaten people in intensive care units and those suffering from cancer, with mortality that can reach an astonishing 40%. The Traven lab is studying how Candida mounts counter-attacks against host immune defences, as well as building molecular knowledge of the fundamental cellular mechanisms that drive fungal virulence and susceptibility to antifungal treatments. In translation-oriented work, Ana’s lab has engaged with engineers and industry partners to characterise novel antimicrobial compounds that have therapeutic potential. The work in the Traven lab has been supported by the NHMRC and ARC.

Microbial pathogens are responsible for millions of deaths globally, with raising concerns over resistance to available therapies (so-called AMR or antimicrobial drug resistance), and predictions suggesting that by 2050 deaths from infections might become more prevalent that deaths from cancer. In addition to bacteria and bacterial “superbugs”, fungal pathogens are another important class of microbes which have become prevalent killers, particularly of immunocompromised and severely ill people. Estimates suggest that at least 1.5 million people die from fungal infections every year. Cancer, HIV, organ transplants and intensive care unit hospitalisation are predisposing factors for life-threatening fungal infections. Compared to bacteria, fungal pathogens are less understood, particularly in relation to their interactions with host immunity and the host-pathogen interplay that determines the outcome of infection. Moreover, fungi are eukaryotes, meaning that their cellular structures and mechanisms of growth, metabolism and division are very similar to human cells. This greatly complicates efforts to develop efficient and safe antifungal therapies that discriminately act on fungal, but not human cells. In fact, only a handful of antifungal drugs are available to treat fungal infections, and issues with them include resistance of the pathogens to therapy, and toxicity to the patient.

The Traven lab focuses on Candida albicans, a common human pathogen that can cause several types of infections that range in seriousness, including oral candidiasis, but also disseminated disease that is highly deadly. The lab is working towards understanding the interactions of Candida with innate immune cells (the first line of defence against fungal overgrowth). For this we use live cell imaging of immune cell-pathogen interactions, mouse infection models and a range of molecular and cell biology approaches. Another major aspect of our work is to define the molecular mechanisms by which Candida albicans is able to transition between developmental phases that are connected to virulence (yeast and hyphal cells), and how it can resist stressors that it encounters during infections (such as antifungal drugs or immune cell attack). Our interests lie in the areas of immunometabolism (i.e. metabolic changes in immune cells and pathogens that control their interactions), and gene expression control (i.e. gene regulatory networks that control the behaviour of Candida in response to the environment).

Over the last 5 years, our work has been funded by the NHMRC and ARC. Recent papers from the lab were published in Cell Metabolism, PLoS Genetics, mBio, Journal of Antimicrobial Chemotherapy and PNAS.