Regulation of HSV-1 infection by the non-homologous end joining machinery (360G-Wellcome-201946_Z_16_Z)

£99,981

DNA viruses, such as Herpes Simplex Virus 1 (HSV-1), exploit specific host DNA repair mechanisms to assist their replication. More recently, the DNA repair machinery that senses damaged self-DNA was shown to function in the innate immune sensing of viral DNA during infection. We aim to understand how a specific DNA repair pathway, non-homologous end joining, affects HSV-1 infection and how this virus exploits or evades these host responses. This work will further our knowledge of cell-intrisic immunity and DNA repair as well as leading to the rational design of improved vaccines and oncolytic viruses. Our preliminary data indicate that two NHEJ proteins, DNA-PKcs and PAXX act to restrict HSV-1 in different ways, via activation of innate immune responses or by directly affecting virus replication. This study will provide the mechanistic basis of these observations and compare these data with the other components of the NHEJ machinery and how they regulate HSV-1 infection. This work will therefore explore two hypotheses: NHEJ proteins regulate innate immune sensing of HSV-1 DNA NHEJ proteins restrict HSV-1 replication in the nucleus

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Grant Details

Amount Awarded 99981
Applicant Surname Ferguson
Approval Committee Science Seeds Advisory Panel
Award Date 2016-04-08T00:00:00+00:00
Financial Year 2015/16
Grant Programme: Title Seed Award in Science
Internal ID 201946/Z/16/Z
Lead Applicant Dr Brian Ferguson
Partnership Value 99981
Planned Dates: End Date 2019-04-01T00:00:00+00:00
Planned Dates: Start Date 2016-10-01T00:00:00+00:00
Recipient Org: Country United Kingdom
Region East of England