Authors: Sally Roberts (University of Birmingham, UK)
In the past, human papillomaviruses (HPVs) have proved a challenge to study owing to a complex life cycle dependent on the infected cell undergoing complete differentiation; however, with the advent of organotypic, three-dimensional (3D) models our understanding of these viruses and the associated cancers has increased.
To learn more, we spoke to Sally Roberts (University of Birmingham, UK) at the recent Microbiology Society Conference (8–11 April, Belfast, UK) about her lab’s models for studying HPV and the virus–host interactions that have been uncovered as a result of this.
First, could you introduce yourself and give a brief summary your career to date?
I am currently at the University of Birmingham as a Senior Lecturer, however, I started off as a biochemistry undergraduate from the University of Warwick (UK). When I graduated, I moved to Oxford (UK) where I worked as research associate at the University for a couple of years and learnt a lot of molecular biology. These were the days before ‘kits’ and so we really had to do everything from scratch!
I then did a PhD in Oxford in the University’s Laboratory of Molecular Biophysics, working on cloning antibodies and engineering the antigen combining site which complexes with the antigen. I was able to publish the work of my thesis in Nature, which was very exciting! Following this, I moved to Birmingham to work on papillomaviruses and since the late 1990s I’ve been a group leader working on the molecular biology of these viruses.
Could you outline the research you’re presenting here?
My work is very much interested in understanding how papillomaviruses replicate in skin cells – keratinocytes. Our research uses primary keratinocytes – the target cell of HPVs – so we are using physiologically relevant cells. This is very important because if you introduce an HPV genome into these cells and differentiate them in 3D organotypic culture you can recapitulate the whole process of the virus life cycle – these viruses only replicate completely when the infected keratinocytes undergoes differentiation.
We are using these models to understand the virus life cycle and the role of virus–host interactions in pathogenesis. We are also interested in using these systems to model HPV infection at anatomical sites where there is a risk of these infections progressing to cancer, such as the tonsil.