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Cambridge Immunology Network



Supervisor: Professor John Sinclair

Following primary infection, HCMV is met with a robust immune response and typically forms a latent infection in cells of the myeloid lineage. Here, the viral genome persists within the latently infected cell with little gene expression and no detectable production of infectious virions. Reactivation from viral latency is pathogenic in immunocompromised individuals such as HIV positive patients, certain cancer patients and organ transplant patients.

I am a first year PhD student working on identifying HCMV-coded proteins expressed by latently infected cells. My aim is to exploit the expression of these proteins to develop new chemical and biological therapies to treat HCMV seropositive patients. In my previous work I focused on using glyco-engineering to develop new methods to overcome the limitations of monoclonal antibody therapy against cancers.


Key publications: 

Baruah K, Bowden TA, Krishna BA, Dwek RA, Crispin M, Scanlan CN. Selective deactivation of serum IgG: a general strategy for the enhancement of monoclonal antibody receptor interactions. J Mol Biol. 2012 Jun 29;420(1-2):1-7.

Goodfellow JJ, Baruah K, Yamamoto K, Bonomelli C, Krishna B, Harvey DJ, Crispin M, Scanlan CN, Davis BG. An endoglycosidase with alternative glycan specificity allows broadened glycoprotein remodelling. J Am Chem Soc. 2012 May 16;134(19):8030-3.

 Benjamin  Krishna
Not available for consultancy


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