alzheimers2FLS researcher Dr Alexander Golovanov, based in the Manchester Institute of Biotechnology, has just obtained an important grant from the US National Institute of Allergy and Infectious Diseases (part of the National Institutes of Health) to understand how the herpes virus infects cells.

The research is being carried out with Professor Rozanne Sandri-Goldin’s world-leading virology group at University of California Irvine USA, and will explore the molecular mechanisms that enable the herpes simplex virus 1 (HSV-1) to hijack the cell and produce more copies of itself.

HSV-1 causes a wide range of diseases, from recurrent painful skin lesions to more serious conditions such as encephalitis. Recent studies by FLS researcher Professor Ruth Itzhaki have suggested that HSV-1 can be a risk factor in the development of Alzheimer’s disease, and that antiviral drugs may therefore be effective at slowing down the progress of Alzheimer’s. Unfortunately, there is a yet not antiviral treatment that can suppress viral replication efficiently enough. Finding a “weak spot” in HSV-1 that could be targeted by future therapies could constitute a significant breakthrough for a number of diseases.

During infection, HSV-1 expresses a protein called ICP27, which helps the virus to take control of the cellular machinery and use it to produce new copies of the virus. Dr Golovanov’s group has previously created the first atomic-level structure of the complex formed by ICP27 and its target in the cell (see: PLOS Pathogens). The new five-year project will look into further details of how the complexes of viral and cellular proteins are organized and regulated and may help to design new drugs that will interfere with this complex assembly and HSV replication.

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