Dr Sally Roberts DPhil

Dr Sally Roberts

Institute of Cancer and Genomic Sciences
Senior Lecturer

Contact details

Institute of Cancer and Genomic Sciences
Institute of Biomedical Research West
College of Medical and Dental Sciences
University of Birmingham
B15 2TT

Sally qualified with a BSc. (Hons) in Biochemistry from the University of Warwick in 1981. She gained a D.Phil from the Laboratory of Molecular Biophysics in the University of Oxford in 1987. She joined the Department of Cancer Studies in the University of Birmingham in 1989, where in 2002 she was promoted to Senior Lecturer.

Sally has published over 50 papers in scientific journals as well as reviews and book chapters in the fields of the molecular biology of the papillomavirus life cycle and papillomavirus driven carcinogenesis. She has received major funding from the Wellcome Trust and Cancer Research UK.


  • DPhil University of Oxford 1987 
  • BSc (Hons) in Biochemistry University of Warwick 1981


Sally came to Birmingham in 1989 with a background in cell and molecular biology and she has since developed a research portfolio studying the molecular biology of human papillomaviruses, small DNA tumour viruses that cause a range of clinical manifestations ranging from anogenital warts and laryngeal papillomas, to cancers as anogenital sites (e.g. cervical cancer) and in the oropharynx.

The molecular basis for such diverse pathogenesis lies in virus-host interactions necessary to support productive infection and Sally’s programme of research focuses on understanding the virus life cycle and the contribution of virus –host interactions to the development of cancer. A centrepiece of her research is the use of physiological three-dimensional epithelial models of the virus life cycle and virus driven carcinogenesis.


Postgraduate supervision

Sally is interested in supervising doctoral research students in the following areas:

  • The molecular biology of the human papillomavirus life cycle
  • The role of human papillomavirus in the pathogenesis of anogenital and oropharyngeal cancers: host-virus interactions that contribute to malignancy


Sally is interested in virus-host interactions that are important in the pathogenesis of human papillomavirus (HPV) infections; driven by the need to improve the understanding of the interactions between HPV and its human host with a view to identifying new therapeutic targets for the treatment of HPV associated disease.

Central to the programme of work is the use of primary keratinocyte – the host cell of the virus - models of viral replication.  Stratification of these models in organotypic raft culture enables recapitulation of the full replication cycle of the virus.  Manipulation of the models in long-term culture reflects virus and host changes observed in the progression of HPV infections to cancer and thus allows investigation of virus-host interactions that contribute to the development of malignancy.  Sally has modeled the virus life cycle in keratinocytes isolated from both the anogenital tract and the oropharynx, to establish a repertoire of physiological models of HPV infection and disease.

Molecular biology of the HPV life cycle

Much of Sally’s earlier HPV research was focused on understanding the functions of the HPV E4 protein that is a major regulator of the virus life cycle.  Her studies have revealed that E4 has multiple functions ranging from suppression of host cellular DNA synthesis to cell cycle dysregulation – functions that may aid virus replication.  More recent work indicates that E4 may regulate viral and host gene expression through potent inhibition of the host kinase SRPK1  - a key regulator of alternative RNA processing.  Emphasis is now on gaining insight into how these multiple actions of E4 contribute to its role in the virus life cycle since the development of a strategy to target E4 function may enable abrogation of virus propagation.

HPV carcinogenesis

HPV induced carcinogenesis is dependent upon interactions between the viral oncoproteins and a number of key cellular pathways controlling cell proliferation and survival.  She is using the cell-based models to understand the importance of the function of the E6 oncoprotein to target cellular PDZ domain-containing proteins (e.g. the tumour suppressor protein discs large 1, that regulate cell proliferation and cell polarity), to the replication cycle of high-risk HPV types.  Sally’s studies of this E6 function have been influential in understanding the contribution of E6 to cellular immortalization, and to how regulation of this E6 function by cellular signalling pathways might contribute to an enhancement of the oncogenicity of the viral protein.

Sally is now using the HPV tonsil replication model to investigate the impact of HPV-host interactions on the development of cancer at this body site.

Sally has key collaborations with other virologists in the Centre for Human Virology in the University of Birmingham ( Dr Joanna Parish) and clinical academics (Professor Hisham Mehanna, Institute of Cancer and Genomic Sciences).

Other activities

  • Member of the Microbiology Society (member of the virology division, 2011 – 2014). 
  • Associate editor (2016 – present), Virology Journal.
  • Member of the editorial board (2015 – present), Pathogen and Infectious Disease.


Most recent publications (full list of publications available at ResearcherID and for open access via erepositories)

Wasson, C. W., Morgan, E. L., Muller, M., Ross, R. L., Hartley, M., *Roberts, S., *Macdonald, A. (2017) Human papillomavirus type 18 E5 oncogene supports cell cycle progression and impairs epithelial differentiation by modulating growth factor receptor signalling during the virus life cycle. Oncotarget https://doi.org/10.18632/oncotarget.21658, published online 6th October 2017 *Equal contribution.

Marsh, E. K., Delury, C. P., Davies, N. J., Weston, C., Miah, M. A. L., Banks, L., Parish, J. L. Higgs, M. R., *Roberts, S. (2017) Mitotic control of human papillomavirus genome-containing cells is regulated by the function of the PDZ-binding motif of the E6 oncoprotein. Oncotarget. Published online 3rd January 2017. DOI: 10.18632/oncotarget.14469.

Harris, L., McFarlane-Majeed, L., Campos Leon, K., Roberts, S., Parish, J. (2017) The cellular DNA helicase ChlR1 regulates chromatin and nuclear matrix attachment of the human papillomavirus type 16 E2 protein and high copy viral genome establishment. J. Virol., 91:e01853-16, doi:10.1128/JVI.01853-16.

Ganti., K., Massimi, P., Manzo-Merino, J., Tomaic, V., Pim, D., Playford, M. P., Lizano, M., Roberts, S., Kranjec, C., Doorbar, J., Banks, L. (2016) Interaction of the human papillomavirus E6 oncoprotein with sorting nexin 27 modulates endocytic cargo transport pathways, PLoSPath, 2016 Sep 20;12(9):e1005854. doi: 10.1371/journal.ppat.1005854.

Knight, G. L., Needham, L., Ward, D., Roberts, S (2016) Pilot study investigating the prevalence of oral human papillomavirus (HPV) infection in young adults. Public Health, published online org/10.1016/j.puhe.2015.12.006.

Leonard, S. M., Pereira, M., Roberts, S., Cuschieri, K., Nuovo, G., San Cassia, P., Athavale, R., Young, L.S. Ganesan, R., Woodman, C. B. (2016) Evidence of disrupted high-risk human papillomavirus DNA in morphologically normal cervices of older women. Scientific Rpts., 6:20847 DOI:10.1038/srep20847.

James, C. D., Roberts, S. (2016) Viral interactions with PDZ domain-containing proteins: an oncogenic trait? Pathogens, 5(1), 8;doi:10.3390/pathogens5010009, published online 18th January 2016.

Mehanna, H., Franklin, N., Compton, N., Robinson, M., Powell, N., Biswas-Baldwin, N., Paeri, V., Hartley, A., Fresco, L., Al-Booz, H., Junor, E., El-Hariry, I., Roberts, S., Harrington, K., Ang, K., Dunn, J., Woodman, C. (2016) Geographic variation in human papillomavirus-associated oropharyngeal cancer: data from four multi-national randomised trials. Head and Neck, doi: 10.1002/hed.24336, published 8th January 2016.

Roberts, S. (2015) Papillomaviruses. In: Encyclopedia of Life Sciences (eLS). John Wiley & Sons, Ltd:Chicehester. DOI:10.1002/9780470015902.a0000422.pub3.

Siddiqa, A., Campos Leon, K., James, C. D., Faraz Bhatti, M., Roberts, S., Parish, J. (2015) The human papillomavirus type 16 L1 protein interacts directly with E2 and enhances E2-dependent replication and transcription activation. J. Gen. Virol., published online 24th April 2015.

Paris, C., Pentland, I., Groves, I., Roberts, D. C., Powis, S. J., Coleman, N., *Roberts, S., *Parish, J. L. (2015) CCCTC-binding factor recruitment to the early region of the human papillomavirus type 18 genome regulates viral oncogene expression. *, co-corresponding author. J. Virol., 89, 4770-4785, published online 18th February 2015, doi:10.1128/JVI.00097-15.

Boon, S-S., Tomaic, V., Thomas, M., Roberts, S., Banks, L. (2015) Cancer-causing human papillomavirus E6 proteins display major differences in the phospho-regulation of their PDZ interactions.  J. Virol., 89, 1579-86, published ahead of print 19th November 2014; doi:10.1128/JVI.01961-14.

Prescott, E. L., Brimacombe, C. L., Hartley, M., Bell, I., Graham, S. V., *Roberts, S. (2014) Human papillomavirus type 1 (HPV1) E1^E4 protein is a potent inhibitor of the serine-arginine (SR) protein kinase SRPK1 and inhibits phosphorylation of host SR proteins and of the viral transcription and replication regulator E2. J. Virol., 88, 12599-611, published ahead of print 20th August 2014, doi:10.1128.

Delury, C. P., Marsh, E. K., James, C. D., Boon, S. S., Banks, L., Knight, G. L., *Roberts, S. (2013) The role of protein kinase A regulation of the E6 PDZ-binding domain during the differentiation-dependent life cycle of human papillomavirus type 18. J Virol, 87, 9463-72, published online June 26th, 2013, DOI 10.1128/JVI.01283-13.

Roberts, S*., Delury, C., Marsh, E. (2012) The PDZ protein discs large (DLG): the “Jekyll and Hyde” of the epithelial polarity proteins. FEBS J, 279, 3549-58, published online Aug 29th 2012 DOI: 10.1111/j.1742-4658.2012.08729.x (invited, peer-reviewed review, front cover article).

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