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  Using live-cell imaging of the immune response to investigate host-pathogen interactions during infection.


   School of Biosciences

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  Prof Robin May  No more applications being accepted  Competition Funded PhD Project (Students Worldwide)

About the Project

My group is interested in the molecular and cellular mechanisms that occur during host-pathogen interactions. In particular, we study phagocytic cells of the innate immune system (macrophages, neutrophils and dendritic cells) in order to understand how it is that some pathogens are able to parasitise these white blood cells.

Our work focuses particularly on fatal human fungal pathogens, with a particular interest in Cryptococcus neoformans (and its close sibling species, C. gattii), a leading cause of death in immunocompromised patients worldwide. We are also interested in rarer, trauma-associated fungal infections and in the enigmatic eukaryotic pathogen Prototheca. We use a combination of cell biology, immunology and genetics to try and understand how these organisms can evade the human immune system.

We monitor immune cell behaviour via high-resolution live cell microscopy, using both tissue culture systems and in vivo work in zebrafish and murine models. In addition, we use genetic approaches (knockouts, transgenics, gene expression analysis and whole genome sequencing) to try and identify novel virulence factors in the pathogen. More information on the group is available at http://www.biosciences-labs.bham.ac.uk/may/Home.html.

If you are an enthusiastic scientist with an interest in host-pathogen interactions, looking for a PhD position to commence in October 2020, we would be happy to hear from you. A background in genetics, cell biology, microbiology or immunology would be helpful, but is not required. A keen and enthusiastic approach to science, together with the ability to take responsibility for your own project within a young, dynamic research team, is essential.

PhD funding is awarded on a competitive basis via Research Council Studentships and Darwin Studentships (all nationalities). Applicants should possess, or expect to be awarded, a high 2.1 or 1st class degree or equivalent.

Funding Notes

Research Council Studentships are available for UK applicants. EU applicants resident in the UK may also be eligible. Non-UK students interested in this project may apply for a Darwin Trust Scholarship. The deadline for applications for Research Council and Darwin Trust studentships is 31st January 2020.

We have a thriving community of International PhD students and encourage applications at any time from students of any nationality either able to fund their own studies or who wish to apply for their own funding (e.g. Commonwealth Scholarship Council, Islamic Development Bank).

For further information on funding see http://www.birmingham.ac.uk/schools/biosciences/courses/postgraduate/phd.aspx

References

RECENT PUBLICATIONS FROM OUR GROUP (for a full list, see http://www.biosciences-labs.bham.ac.uk/may/Home.html)

Gilbert et al. Vomocytosis of live pathogens from macrophages is regulated by the atypical MAP kinase ERK5. Science Advances, 2017

Farrer et al. Microevolutionary traits and comparative population genomics of the emerging pathogenic fungus Cryptococcus gattii. Phil Trans Roy Soc B, 2016

Samantaray et al. Novel cell-based in vitro screen to identify small-molecule inhibitors against intracellular replication of Cryptococcus neoformans in macrophages. Int J Antimicrobial Agents, 2016.

Voelz et al. 'Division of Labour' in response to host oxidative burst drives a fatal Cryptococcus gattii outbreak. Nature Communications 2014

Sabiiti et al. Efficient phagocytosis and laccase activity affect the outcome of HIV-associated cryptococcosis. Journal of Clinical Investigation, 2014

Voelz et al. Transmission of Hypervirulence Traits via Sexual Reproduction within and between Lineages of the Human Fungal Pathogen Cryptococcus gattii. PLOS Genetics 2013

Johnston SA, May RC. The human fungal pathogen Cryptococcus neoformans escapes macrophages by a phagosome emptying mechanism that is inhibited by Arp2/3 complex-mediated actin polymerisation. PLoS Pathogens. 2010

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