Professor Ursula Gompels BA MA MSc PhD
- Ursula Gompels's Contacts
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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.
- Child health
- Innate immunity
- Maternal health
- Neonatal health
- Cell biology
- Molecular biology
Disease and Health Conditions
- Emerging Infectious Disease
- European Union
- Sub-Saharan Africa (developing only)
- Czech Republic
- New Zealand
- United Kingdom
- United States
- Capacity Development
- Cell Signalling
- Cell Surface Receptors
- Cellular Immunology
- Child Development
- Commonwealth countries
- Emerging Infectious Diseases
- Maternal And Child Health
- Neonatal Survival
- Next Generation Sequencing
- Opportunistic Infectious Diseases
- host virus interactions
Complete Genome Sequence of Germline Chromosomally Integrated Human Herpesvirus 6A and Analyses Integration Sites Define a New Human Endogenous Virus with Potential to Reactivate as an Emerging Infection.
Tweedy, J. ; Spyrou, M.A. ; Pearson, M. ; Lassner, D. ; Kuhl, U. ; Gompels, U.A. ;
Viruses, 2016; 8(1)
Increased Cytomegalovirus Secretion and Risks of Infant Infection by Breastfeeding Duration From Maternal Human Immunodeficiency Virus Positive Compared to Negative Mothers in Sub-Saharan Africa.
Musonda, K.G.; Nyonda, M.; Filteau, S.; Kasonka, L.; Monze, M.; Gompels, U.A.;
J Pediatric Infect Dis Soc, 2016; 5(2):138-46
Analyses of Germline, Chromosomally Integrated Human Herpesvirus 6A and B Genomes indicate Emergent Infection and new Inflammatory Mediators.
Tweedy, J.; Spyrou, M.A.; Hubacek, P.; Kuhl, U.; Lassner, D.; Gompels, U.A.;
J Gen Virol, 2015; 96(Pt 2):370-89
Reduced Poliovirus vaccine neutralising-antibody titres in infants with maternal HIV-exposure.
Sanz-Ramos, M.; Manno, D.; Kapambwe, M.; Ndumba, I.; Musonda, K.G.; Bates, M.; Chibumbya, J.; Siame, J.; Monze, M.; Filteau, S.; Gompels, U.A.; CIGNIS study team, .;
Vaccine, 2013; 31(16):2042-9
Activation of CCR2+ human proinflammatory monocytes by human herpesvirus-6B chemokine N-terminal peptide.
Clark, D.J.; Catusse, J.; Stacey, A.; Borrow, P.; Gompels, U.A.;
J Gen Virol, 2013; 94(7):1624-35
Human Cytomegalovirus Infant Infection Adversely Affects Growth and Development in Maternally HIV-Exposed and Unexposed Infants in Zambia.
Gompels, U.A. ; Larke, N. ; Sanz-Ramos, M. ; Bates, M. ; Musonda, K. ; Manno, D. ; Siame, J. ; Monze, M. ; Filteau, S. ; the CIGNIS Study Group, . ;
Clin Infect Dis, 2012; 54(3):434-442
Immunomodulation by herpesvirus U51A chemokine receptor via CCL5 and FOG-2 down-regulation plus XCR1 and CCR7 mimicry in human leukocytes.
Catusse, J.; Spinks, J.; Mattick, C.; Dyer, A.; Laing, K.; Fitzsimons, C.; Smit, M.J.; Gompels, U.A.;
Eur J Immunol, 2008; 38(3):763-777
Inhibition of HIV-1 infection by viral chemokine U83A via high affinity CCR5 interactions which block human chemokine-induced leukocyte chemotaxis and receptor internalisation.
Catusse, J.; Parry, C.M.; Dewin, D.R.; Gompels, U.A.;
Blood, 2007; 109(9):3633-9
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