Professor Ursula Gompels
BA MA MSc PhD
in Molecular Virology
University of Cambridge for PhD and postdoctoral studies at the MRC National Institute for Medical Research and Cambridge training in herpesvirus molecular biology. Awarded a Wellcome Trust Senior Research Fellowship in the Department of Medicine, Cambridge, then appointed as faculty in LSHTM. Awarded a Royal Society Industry Fellowship at GlaxoSmithKline in 1999, returned to LSHTM in 2003 and appointed Reader then Professor in Molecular Virology.
Chair Exam Board: MSc Molecular Biology of Infectious Diseases (MBID)
Course committees and exam boards: MSc Molecular Biology of Infectious Diseases (MBID) and Medical Microbiology (MM).
Study Unit Organiser: Core Virology (3121) and Molecular Virology(3140)
Supervision and Examiner: PhD; MSc MBID, MM
Research is on the human herpesvirus family with current focus on the betaherpesvirus subgroup including human herpesvirus 6A and 6B (HHV-6A and B) and human cytomegalovirus (HCMV). These viruses can be significant pediatric pathogens and are major opportunistic infections in immune suppressed HIV/AIDS and transplantation patients causing both morbidity and mortality. HHV-6A and B are also linked with neuro-inflammatory disease and both uniquely can integrate their genomes into human subtelomeres in the germ line of approximately 1.0% of people worldwide; giving the potential to express virus genes in every cell. We have defined novel genomes integrated as new endogenous virus with capacity to reactivate as emergent infections. Herpesviruses cause latent infections which persist for life, thus their intimate adaptations to our immune system provide unique tools to understand host-pathogen interactions.
Work covers areas in infection and immune mediation as well as adaptation to gene therapeutic systems: i) genomic variation in infection modulators in relation to pediatric disease, with collaborative links with the University Teaching Hospital in Zambia, including particular interests in adverse development effects we have demonstrated on maternally HIV-exposed children; ii) studies on molecular mechanisms of postnatal virus entry or gene delivery mediated by cell fusion or congenital by genomic integration and iii) characterisation of viral versions of the inflammatory mediators, chemokine and chemokine receptors, as major components of immunomodulation. Our studies have identified and characterised the virus chemokine receptor and chemokines. We showed the virus chemokines can also efficiently inhibit HIV infection. Overall, the virus chemokines and receptors can mimic or prevent cellular signalling and thereby direct immune cell recruitment/activation; with applications to immunotherapeutics, vaccine responses and control of inflammatory disease. These are being adapted to novel viral vectors which can affect DNA vaccines and gene delivery.