Matthias T. Dittmar

Matthias T Dittmar

Non-Clinical Senior Lecturer in Virology

We are seeking to identify novel antiviral targets to develop new treatment options, as well as predictive markers to manage infections more successfully. Viruses are obligatory cellular parasites, with their replication crucially depending on host cell functions. They have evolved strategies to modulate host cell cytoskeleton dynamics, activate signal transduction pathways to facilitate entry into new target cells and modify the proteome and RNAome to overcome cellular antiviral responses.

Therefore, viruses are ideal tools to study signalling and cytoskeleton networks and proteome/RNAome in an integrative way by comparing the dynamics of such virus exploited networks. With the increasing knowledge regarding the regulation of these networks it is now feasible to identify in more detail the host machineries that certain viruses hijack to further replication. Therefore, viruses like HIV and HCV will be tremendously useful in the emerging field of molecular systems biology leading to the identification of novel targets to develop new treatment options as well as predictive markers to manage infections more successfully.

Recent and ongoing research projects:

Virogenomics in HCV infection:
Hepatitis C virus (HCV) infection is globally widespread and is an increasing cause of severe liver disease and mortality (cirrhosis and hepatocellular carcinoma). In the UK at least 150,000 individuals are chronically infected and a large proportion will develop end stage liver disease without treatment. The UK HCV population is more diverse than that seen in other countries (reflecting ethnic heterogeneity) and, unlike other developed countries, genotype 3 is common. Recent research has identified a growing number of large and small noncoding RNA’s (ncRNA: large intergenic- and micro-RNA) that are expressed in mammalian cells. These noncoding RNA’s regulate a large fraction of the transcriptome and facilitate innate responses. This multi-gene regulatory capacity enables remodelling of the signalling landscape and innate responses to viral pathogens in a timely and translation-independent manner. Studying virus induced ncRNA profiles from patient cohorts infected with different HCV genotypes, grouped into progressor and non-progressor will reveal any significant differences in ncRNAs and has the potential to identify predictive markers for progression. Comparison of pre-treatment profiles of patients who did or did not respond to therapy may provide insights into profiles that predict treatment outcome.

Quantification of HIV and HCV envelope dependent changes in signalling and cytoskeleton networks:
This project focuses on integrated cellular responses upon viral envelope-receptor interactions. We compare cell-cell interaction as well as virus-cell interaction for two different viruses (Human Immunodeficiency Virus and Hepatitis C Virus, HIV and HCV) to identify common and distinct cellular responses. Exploiting state of the art imaging technologies we are currently characterising the dynamic changes (temporal and spatial) in cellular networks such as signalling pathways and cytoskeleton rearrangements. This knowledge will inform target identification to develop specific or broad acting antiviral drugs.


Matthias joined the Blizard Institute in 2007 as Senior Lecturer after successfully leading his own research groups at Heinrich-Pette-Institute/Hamburg and Institute of Virology/Heidelberg for 9 years. He is a biochemist by training, working on Simian Immunodeficiency Viruses during his PhD, followed by a post-doctoral fellowship to work on HIV cell entry at the Institute of Cancer Research/London from 1995 to 1997.

Matthias is a Senior Fellow of the Higher Education Academy and has been appointed SMD faculty Mentor for Academic Development for the Blizard Institute.


  • Virogenomics in HCV infection
  • Quantification of HIV and HCV envelope dependent changes in signalling and cytoskeleton networks


Malinowsky, K., Luksza, J., and Dittmar, M.T. (2008). Susceptibility to virus-cell fusion at the plasma membrane is reduced through expression of HIV gp41 cytoplasmic domains. Virology 376: 69-78

Kaumanns, P., Hagmann, I., and Dittmar, M.T. (2006). Human TRIM5alpha mediated restriction of different HIV-1 subtypes and Lv2 sensitive and insensitive HIV-2 variants. Retrovirology 3:79 (6Nov2006)

Neumann, T., Hagmann, I., Lohrengel, S., Heil, M.L., Derdeyn, C.A., Kräusslich, H.-G., and Dittmar, M.T. (2005). T20 insensitive HIV-1 from naive patients exhibits high viral fitness in a novel dual colour competition assay on primary cells. Virology 333: 251-262.

Daecke, J., Fackler, O.T., Dittmar, M.T. and Kräusslich, H.-G. (2005). Involvement of clathrin mediated endocytosis in HIV-1 entry. J. of Virology 79: 1581-1594.

View all Matthias Dittmar's Research Publications at:


Programme Lead, intercalated BSc Infectious Disease and Epidemiology
Co-lead for the Graduate Entry Programme module Infection and Immunity                                                                                                
Module Lead for Y2 and Y3 Biomedical Sciences Case Approach module, BSc Biomedical Sciences
Module Lead (Virology), MSc Clinical Microbiology
Taught modules: MBBS, year 1 to 4 (FunMed, CSP, Problem Based Learning, SSC2/4)

Topics for PhD supervision:

HIV entry and the cytoskeleton

Further information

Development of virus trump cards and viral infection based games for the Centre of the Cell


Centre for Immunology and Infectious Disease
Blizard Institute
Barts and The London School of Medicine and Dentistry
Blizard Building
4 Newark Street
E1 2AT

Centre Administrator: Jaya Rajamanie
020 7882 2329
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