Professor Jane McKeating B.Sc. PhD

Professor of Molecular Virology

School of Immunity and Infection

Contact details

Telephone +44 (0)121 414 8173

Fax +44 (0)121 414 3599

Email j.a.mckeating@bham.ac.uk

School of Immunity and Infection
College of Medical and Dental Sciences
Medical School Building
University of Birmingham
Edgbaston
Birmingham
B15 2TT
UK

About

Jane McKeating is the Professor of Molecular Virology.

She set up the HCV group at the Medical School in January 2005. The group occupies 3 adjoining labs on the 5th floor of the IBR, 2 cat 3 labs and have shared access to all of the facilities in the MRC Centre for Immune Regulation. The group is involved in a wide range of local and international collaborative studies.

Qualifications

  • PhD 1987
  • BSc (Hons) 198

Teaching

TEACHING PROGRAMMES

Postgraduate supervision

The HCV group is actively involved in the supervision and mentoring of doctoral research (Ph.D.) students in the all areas of clinically relevant HCV disease.

If you are interesting in studying in this area please contact us using the contact details above, or for more general doctoral research enquiries, please email: dr@contacts.bham.ac.uk or call +44 (0)121 414 5005.

For a full list of available Doctoral Research opportunities, please visit our Doctoral Research programme listings

Research

RESEARCH THEMES
Viral hepatitis, virus entry and viral Oncology

RESEARCH ACTIVITY
Our research focus is to understand critical events associated with early infection pathway(s) of clinically significant viruses, human immunodeficiency virus (HIV) and hepatitis C virus (HCV). We applied our expertise in retrovirus assembly to develop HIV-based pseudoparticles (HCVpp) expressing HCV glycoproteins, providing a long-awaited culture system to study the mechanism of HCV tropism for hepatocytes and to identify entry inhibitors. HCVpp enabled us to demonstrate the essential role of CD81 and scavenger receptor BI in virus entry and to discover that tight junction proteins Claudin-1 and Occludin were required for productive infection of hepatocytes. Recent advances in the development of an in vitro culture system that support the replication and assembly of infectious HCV genomes have allowed studies on the complete viral lifecycle. Current work in the laboratory studies the role of viral diversity in HCV dissemination and pathogenesis. Recent studies from our laboratory show that HCV can spread by cell-free particle infection of naïve cells and via direct cell-to-cell spread. Importantly, cell-free and cell-to-cell routes of HCV infection show different sensitivities to neutralizing anti-viral antibodies and immune modulators such as interferon alpha, supporting the importance of cell-to-cell transmission in immune evasion.

Other activities

Awards and Distinctions:

Herpes Vaccine Research Trust Prize, Society of General Microbiology - 1988.

Medical Research Council Senior AIDS Research Fellowship -1990

Research Fellowship of the Lister Institute of Preventive Medicine - 1994

Fleming Award, Society of General Microbiology - 1995.
Royal Society Wolfson Merit Award 2006

Australian ACH2 Inivited Lecture 2009

Oxford University Distinguished Virology Lecture 2010

Dutch Society of Hepatology Distinguished Lecture – 2011

Membership of committees & boards:

NIH special study section on Virology

Veterans Administration Merit Review Subcommittee.

Editorial boards for Virology, Virology Journal, PLos One, Hepatology

Scientific Advisory Boards for University of Essen, Astex Pharmaceuticals and Arrow Pharmaceuticals

Publications

Neutralizing antibody-resistant hepatitis C virus cell-to-cell transmission. Brimacombe CL, Grove J, Meredith LW, Hu K, Syder AJ, Flores MV, Timpe JM, Krieger SE, Baumert TF, Tellinghuisen TL, Wong-Staal F, Balfe P, McKeating JA
Journal of virology 2011 85: 596-605

Small molecule scavenger receptor BI antagonists are potent HCV entry inhibitors. Syder AJ, Lee H, Zeisel MB, Grove J, Soulier E, Macdonald J, Chow S, Chang J, Baumert TF, McKeating JA, McKelvy J, Wong-Staal F
Journal of hepatology 2011 54: 48-55

Hepatitis C virus infection of neuroepithelioma cell lines. Fletcher NF, Yang JP, Farquhar MJ, Hu K, Davis C, He Q, Dowd K, Ray SC, Krieger SE, Neyts J, Baumert TF, Balfe P, McKeating JA, Wong-Staal F
Gastroenterology 2010 139: 1365-74

Claudin association with CD81 defines hepatitis C virus entry. Harris HJ, Davis C, Mullins JG, Hu K, Goodall M, Farquhar MJ, Mee CJ, McCaffrey K, Young S, Drummer H, Balfe P, McKeating JA
The Journal of biological chemistry 2010 285: 21092-102

Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor-dependent manner. Mee CJ, Farquhar MJ, Harris HJ, Hu K, Ramma W, Ahmed A, Maurel P, Bicknell R, Balfe P, McKeating JA
Gastroenterology 2010 138: 1134-42

Hepatoma cell density promotes claudin-1 and scavenger receptor BI expression and hepatitis C virus internalization. Schwarz AK, Grove J, Hu K, Mee CJ, Balfe P, McKeating JA
Journal of virology 2009 83: 12407-14

Polarization restricts hepatitis C virus entry into HepG2 hepatoma cells. Mee CJ, Harris HJ, Farquhar MJ, Wilson G, Reynolds G, Davis C, van IJzendoorn SC, Balfe P, McKeating JA
Journal of virology 2009 83: 6211-21

Mutations in hepatitis C virus E2 located outside the CD81 binding sites lead to escape from broadly neutralizing antibodies but compromise virus infectivity. Keck ZY, Li SH, Xia J, von Hahn T, Balfe P, McKeating JA, Witteveldt J, Patel AH, Alter H, Rice CM, Foung SK
Journal of virology 2009 83: 6149-60

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