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Employing molecular virology to investigate hepatitis E virus replication


   Faculty of Biological Sciences


About the Project

Hepatitis E virus (HEV), is a major causative agent of acute, severe hepatitis. The infection can also be chronic, particular in immunocompromised people, and fatal in pregnant women or those with existing liver diseases. The virus can be zoonotic (i.e. it can spread from animals to humans) and can infect a wide range of animals, most notable pigs where it can be passed onto humans through consumption of contaminated pork products. There are no licenced therapies to treat HEV infection and therefore there is a requirement to develop new therapeutic strategies.

Until recently, probing details of HEV replication has been challenging, partly due to the lack of suitable reagents. This project aims to exploit recently developed subgenomic replicons and and infectious molecular clones to understand the function of the viral non-structural proteins on a molecular level (in combination with biochemical, labelling and state-of-the-art imaging approaches). These proteins are unique to the virus and essential for viral genome replication. Therefore, they make ideal targets for the design of new therapeutics. The long-term aim of the work is to use a greater knowledge of the molecular details of viral replication to develop new approaches for disease control and diagnosis.


References

Herod MR, Ward J, Tuplin A, Harris M, Stonehouse NJ, McCormick CJ. 2022. Positive strand RNA viruses differ in the constraints they place on the folding of their negative strand. RNA. 079125.122
Adeyemi OO, Ward JC, Snowden JS, Herod MR, Rowlands DJ, Stonehouse NJ. 2021. Functional advantages of triplication of the 3B coding region of the FMDV genome. The FASEB Journal. 35(2).
Snowden JS, Hurdiss DL, Adeyemi OO, Ranson NA, Herod MR, Stonehouse NJ. 2020. Dynamics in the murine norovirus capsid revealed by high-resolution cryo-EM. PLOS Biology. 18(3).
Herod MR, Adeyemi OO, Ward J, Bentley K, Harris M, Stonehouse NJ, Polyak SJ. 2019. The broad-spectrum antiviral drug arbidol inhibits foot-and-mouth disease virus genome replication. The Journal of General Virology. 100(9), pp. 1293-1302.
Herod MR, Gold S, Lasecka-Dykes L, Wright C, Ward JC, McLean TC, Forrest S, Jackson T, Tuthill TJ, Rowlands DJ, Stonehouse NJ. 2017. Genetic Economy in Picornaviruses: Foot-and-Mouth Disease Virus Replication Exploits Alternative Precursor Cleavage Pathways. PLoS Pathogens. 13(10).
Herod MR, Liu M, McCormick CJ, Schregel V, Hinds C, McLauchlan J. 2014. Genetic complementation of hepatitis C virus nonstructural protein functions associated with replication exhibits requirements that differ from those for virion assembly. Journal of Virology. 88(5), pp. 2748-2762.

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