Henry Blest

The host’s immune system acts to restrict viral invasion. Equally viruses encode antagonists of the host immune response to allow replication. I am captivated by intriguing molecular narratives created during the game of cat and mouse between virus and host. 

I completed my Bsc (Hons) in Natural Sciences at the University of Leeds screening FDA approved drugs for activity against emerging viruses. Subsequently I studied virology and immunology (Msc) at UCL working on the innate immune response to both human immunodeficiency virus (HIV) and human cytomegalovirus (HCMV).

I was awarded funding through the WIMM studentship (MRC) to join the Rehwinkel Group in 2018 to study the mechanics by which cells detect the genomes of incoming viruses through pattern recognition receptors. My work has focussed on how Herpes Simplex 1 (HSV-1) evades detection by STING and so hides from the hosts innate immune response principally the antiviral cytokine interferon. Although operational DNA sensing is required for protection from viral threat, overzealous responses drive chronic proinflammatory conditions. For example, the rare and debilitating interferonopathy - Aicardi- Goutieres syndrome (AGS) – is driven by chronic activation of the STING pathway. Additionally, in other more prevalent autoimmune disorders such as systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease STING signalling is thought to contribute to pathology. Research into how viruses antagonise the host consistently reveals previously unknown immune components and mechanisms. Pharmaceutical manipulation of newly identified facets of the innate immune response could be used to treat the aforementioned autoimmune conditions. Additionally, STING agonists are sought after for cancer immunotherapy as they show potent antitumour effects in vivo. My work uses viruses as tools to identify new facets of cGAS-STING pathway and so novel drug targets.