Dr Joanna Parish BSc, PhD

Dr Joanna Parish

Institute of Cancer and Genomic Sciences
Senior Lecturer

Contact details

Institute of Cancer and Genomic Sciences
Centre for Human Virology
IBR West
University of Birmingham
B15 2TT

Dr Jo Parish was awarded a Royal Society University Research Fellowship in 2007 and was appointed Senior Lecturer in Institute of Cancer and Genomic Sciences at the University of Birmingham in 2012.

The main focus of Jo’s research is the study of novel virus-host interactions that are important for viral pathogenesis and persistence. Jo has a longstanding interest in the molecular biology of human papillomavirus (HPV) life cycle and uses state-of-the art model systems and technologies to study HPV replication, persistence and transcriptional control.  


  • PhD in Biochemistry, University of Bristol, 2002
  • BSc in Biochemistry, University of Bristol, 1998


Dr Jo Parish is a Royal Society University Research Fellow and Deputy Director of the Centre for Human Virology at the University of Birmingham, UK. 

Jo completed her Ph.D. at University of Bristol in 2002, during which she elucidated the mechanism of the induction of apoptosis by the HPV E2 protein under the supervision of Dr. Kevin Gaston. Following her Ph.D. studies, she moved to the University of Massachusetts Medical School, USA to work with Professor Elliot Androphy. During this time, Joanna continued her study of the papillomavirus E2 protein and discovered several novel virus-host interactions including an interaction with the cellular DNA helicase ChlR1. Her work elegantly demonstrated that ChlR1 is required for the maintenance and persistence of papillomavirus by tethering viral genomes to cellular chromatin during mitosis and was published in Molecular Cell. In 2007, Joanna was awarded a highly competitive Royal Society University Research Fellowship and returned to the UK to establish her independent research group at the University of St Andrews. Joanna was recruited to the University of Birmingham, UK in 2012 and is Group Leader of the HPV Persistence Group. Joanna is a passionate mentor of early career researchers and as an elected member of the Microbiology Society Virus Division continues to promote virology on a national and international stage.

Dr Parish’s research is currently focused on the molecular biology of HPV persistence and the study of virus host-interactions that are important for transcriptional control and persistence of HPV and other small DNA viruses. Her recent research has identified an essential role for the host transcription factor CTCF in the control of differentiation-dependent virus gene expression and she continues to address long-standing questions about HPV gene expression control and replication using novel and state-of-the-art technologies. 


  • Deputy module organiser BMedSci: Viruses Threats and Defences
  • Lecturer and Tutor for BMedSci years 1 and 2 ‘Infection and Immunity’
  • Lecturer for BMedSci (Clinical Sciences)
  • MBChB Tutor: ‘Cancer: Causes to Cures’

Postgraduate supervision

Dr Jo Parish has supervised more than 10 postgraduate students in areas of virology and cancer biology. Many of these students now hold posts at prestigious national and international research intitutes.

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

  • Regulation of HPV gene expression control
  • Regulation of HPV replication and persistence
  • Regulation of HBV gene expression control

If you are interested in studying any of these subject ares please contact Jo using the details above or for any general doctoral research enquiries, please email: dr@contacts.bham.ac.uk or call +44 (0)121 414 5005


Research Theme

Dr Parish’s research programme aims to understand the mechanistic underpinnings of virus gene expression control, replication and persistence using physiological models of human papillomavirus (HPV) and hepatitis B virus (HBV) infections.

Current projects:

Virus-host interactions important for the control of HPV gene expression and HPV-induced carcinogenesis
Using primary keratinocyte-based models of HPV infections, we are characterizing novel host factors that are important for virus oncogene expression and differentiation-dependent regulation of HPV gene expression. Our collaborative work with Dr Sally Roberts has highlighted an important interaction between HPV and the host cell transcriptional regulator CTCF in the control of virus oncogene expression and we are currently analysing this interplay in HPV-induced disease progression. Work is supported by CR-UK, MRC and The Royal Society

 Viral manipulation of host cell gene expression
Using state-of-the-art technologies such as RNA-Seq, ChIP-Seq and FAIRE-Seq we are discovering how HPV manipulates transcriptional control of host cell genes to support virus life cycle. These studies are increasing our understanding of how HPV infection contributes to cancer development and will inform the design of novel diagnostic and prognostic biomarkers. Work is supported by CR-UK and MRC.

Host factors that facilitate virus replication
We are characterizing several novel HPV-host interactions that are important in the control of HPV replication and productivity. Previous work in the Parish group has highlighted an essential role of the DNA helicase ChlR1 in the persistence of HPV episomes by facilitating tethering of episomes to host cell chromosomes during mitotic cell division. We are continuing this work to further understand the function of ChlR1 in viral genome replication and tethering in the HPV life cycle.

We are also interested in how HPV targets the cellular replication machinery and DNA damage response pathways to support viral DNA replication. We are studying novel virus interactions with these cellular pathways using primary keratinocyte-based models of the HPV life cycle and a variety of innovative cell biology techniques. Work is supported by The Royal Society.

Virus-host interactions important for the control of HBV gene expression.
We are studying host cell-mediated regulation of HBV gene expression using physiologically-relevant models of HBV infection and state-of-the-art technologies. 

Other activities

  • Associate Editor of Viruses (2016 - present)
  • Guest Editor of Viruses Special Issue: Tumour Viruses http://books.mdpi.com/978-3-03842-152-8
  • Editorial Board member of Journal of General Virology (2015- present)
  • Elected member of the Microbiology Society Virus Division Committee (2015-present)
  • Member of the American Society for Microbiology
  • Member of the British Society for Cell Biology
  • Member of the Biochemical Society


Most recent publications (full list of publications available at ResearcherID)

Marsh E, Delury C, Davies N, Weston C, Miah ML, Banks L, Parish JL, Higgs M and Roberts S. Mitotic control of human papillomavirus genome-containing cells is regulated by the function of the PDZ-binding motif of the E6 oncoprotein. Oncotarget. 2017; DOI: 10.18632/oncotarget.14469

Campos Leon K, Wijendra K, Siddiqa A, Pentland I, Feeney K, Knapman A, Davies R, Androphy E and Parish JL. Association of human papillomavirus type 16 E2 with Rad50-interacting protein 1 enhances viral DNA replication: Rint1 participates in HPV DNA replication. Journal of Virology. 2017; 91 (5):1-15.

Harris L, McFarlane L, Campos Leon K, Roberts S and Parish JL. 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: ChlR1 regulates the chromatin association of HPV16 E2. Journal of Virology. 2017; 91(1):1-16.

Siddiqa, A., Campos-Leon K., James, C., Roberts, S., Parish, J.L. The human papillomavirus type 16 L1 protein interacts with E2 and enhances E2-dependent replication and transcription activation. Journal of General Virology. 2015; 96, 2274-2285. DOI: 10.1099/vir.0.000162

Pentland, I Parish, J.L. Targetting CTCF to control virus gene expression:A common theme amongst diverse DNA viruses. (2015) Viruses. 7(7):3574-85. doi: 10.3390/v7072791

Paris, C., Pentland, I., Groves, I., Roberts, D.C., Coleman, N., Roberts, S. and Parish J.L. CCCTC-Binding Factor Recruitment to the Early Region of the Human Papillomavirus Type 18 Genome Regulates Viral Oncogene Expression. Journal of Virology. 2015;89(9):4770-85. Cover Image DOI: 10.1128/JVI.00097-15

Siddiqa A, Zainab M, Qadri I, Bhatti MF, and Parish J.L. Prevalence and genotyping of high risk human papillomavirus in cervical cancer samples from Punjab, Pakistan. Viruses 2014; 6, 2762-2777. DOI: 10.3390/v6072762

Prystowsky M. B., Feeney K. M., Kawachi N., Montagne C., Willmott M. K. S., Wasson C. W., Antkowiak M., Loudig O. and Parish J. L. Inhibition of Plk1 and Cyclin B1 expression results in panobinostat-induced G2 delay and mitotic defects. Scientific Reports. 2013;3:2640. DOI: 10.1038/srep02640

Feeney K. M., Saade A., Okrasa K. and Parish J. L. In vivo analysis of the cell cycle dependent association of the bovine papillomavirus E2 protein and ChlR1. Virology. 2011;414:1-9. DOI: 10.1016/j.virol.2011.03.015

Jolly C. E., Gray L. J., Parish J. L., Lain S. and Herrington C. S. Leptomycin B Induces Apoptosis in Cells Containing the Whole HPV 16 Genome. The International Journal of Oncology. 2009;35:649-656.

Prystowsky M. B., Adomako A., Smith R. V., Kawachi N., McKimpson W., Atadja P., Chen Q., Schlecht N., Parish J. L., Childs G. and Belbin T. The histone deacetylase inhibitor LBH589 inhibits expression of mitotic genes causing G2/M arrest and cell death in head and neck squamous cell carcinoma cell lines. Journal of Pathology. 2009;218 (4):467-477.

Parish J. L., Bean A.M., Park R.B., Androphy E.J. ChlR1 is required for loading papillomavirus E2 onto mitotic chromosomes and viral genome maintenance. Molecular Cell. 2006;24(6), 70-76.

Parish J. L., Rosa J., Wang X., Lahti J., Doxsey S. J., Androphy E. J. The DNA helicase ChlR1 is required for sister chromatid cohesion in mammalian cells. Journal of Cell Science. 2006;119, 4857-4865.

Parish J. L., Kowalczyk A., Chen H-T., Roeder G., Sessions R., Buckle M. and Gaston K.  The E2 proteins from high- and low-risk HPV type differ in their ability to bind p53 and induce apoptotic cell death. Journal of Virology. 2006;80 (9), 4580-90.