Understanding the pathogen responsible for COVID19 through genetic, genomic and functional analyses

Virology Team

Ian Goodfellow

Current work focuses on the proteomic analysis of the components of the calicivirus translation initiation complex, structural analysis of the roles of other translation initiation factors in calicivirus translation, as well as the identification of inhibitors of this novel translation mechanism as potential anti-viral therapeutics. Identification and characterisation of RNA-protein interactions required for calicivirus replication.

This project aims to identify the cis-acting functional RNA structures within the viral genome as well as the viral and host cell proteins which interact with these structures, and then to subsequently determine the role of these interactions in the norovirus life cycle. This will not only give us a greater insight into how these viruses replicate but will also lead to the identification of method for rationale attenuation of noroviruses.

Mark Wills

My research interests are in understanding how the human immune system fights virus infections. I have a particular interest in the parts of the immune system that uses cytotoxic killer cells to identify cells in the body that have been infected by a virus and are then be able to kill that cell without damaging healthy cells around the infected cell. These killer cells include T cells and Natural Killer cells.

In my usual research I work on a virus called Human cytomegalovirus (HCMV) a member of the Herpesvirus family, we seek to addressed a number of important questions concerning the immunobiology of HCMV during infection and how this virus uses immune evasion mechanism. Our clinical aim is to discover mechanisms that we can use to eliminate the virus once someone has been infected with it.

In our COVID19 research we will be utilizing our knowledge of immune responses to viruses to look at the COVID19 specific T cell responses in patients with mild to very serious disease, to further understand the contribution of this critical arm of the immune response. Identifying what parts of the virus that these T cells target in patients who have made effective immune responses is important in understanding how best to design a vaccine.

Ewan Harrison

I am Career Development Fellow on a UKRI Innovation Fellowship as part of Cambridge Health Data Research (HDR) UK substantive site. I am also a Senior Research Associate in the Department of Medicine and a Honorary Fellow in the Department of Public Health and Primary Care at the University of Cambridge.  I completed my PhD in 2010 on the genomics and pathogenesis of the opportunistic pathogen Pseudomonas aeruginosa. My post-doctoral work at the University of Cambridge focused on the analysis of Methicillin-resistant Staphylococcus aureus (MRSA) populations in animals and humans and tracking the transmission of MRSA in healthcare facilities using both computational and laboratory-based approaches. 

My current research focuses on the biology of S. aureus. In particular, I am interested in the biological basis of persistent nasal colonisation. To do this I am combining large cohort-based studies, microbiome sequencing, conventional microbiology and electronic health record data. I am also interested in understanding and overcoming mechanisms of beta-lactam resistance in S. aureus


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