Viruses do not encode their own protein synthesis machinery, but must hijack that of their host cell. Viral mRNAs are vastly outnumbered by cellular mRNAs and therefore many viruses have evolved novel mechanisms to preferentially recruit ribosomes. We are interested in the mechanisms by which retroviruses such as HIV are able to recruit ribosomes to their RNAs at the right time to make the proteins they need for new viral particles.

Due to the compact nature of their genomes, many viruses encode several proteins from one mRNA. We are also interested in the mechanisms that viruses employ to direct translation of different proteins from one RNA molecule.

Understanding of these novel translation mechanisms will not only open up new avenues for treatment of viral infection, but also shed light on cellular protein synthesis. Loss of control of cellular translation has been shown to contribute to diseases such as diabetes and cancer.

Current Research Projects:

Comparison of gene expression between HIV-1 and HIV-2
The role of matrix protein in HIV-1 and HIV-2
The interaction of HIV-1 Gag with cellular protein trafficking pathways
IRES-dependent translation in human rhinoviruses
Unr as a master regulator of cellular translation

Lab Members:

Justine Alford
Gemma Watkins
Michela Marongiu

Funding Sources:

Medical Research Council
Biotechnology and Biological Sciences Research Council

Research Collaborations:

Dr Robert Spooner, School of Life Sciences, University of Warwick
Dr Paul Digard, Department of Pathology, University of Cambridge
Dr Ed Anderson, Department of Chemistry, University of Oxford
Prof. Andrew Lever, Department of Medicine, University of Cambridge
Prof. Anne Willis, School of Pharmacy, University of Nottingham