基本信息
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职业迁徙
个人简介
In 2011, I completed my PhD in herpesvirus biology at the University of Cambridge. I then gained experience in circadian biology working as a post-doctoral research associate at the Institute of Metabolic Science, University of Cambridge, and subsequently as an Investigator Scientist at the MRC Laboratory of Molecular Biology.
RESEARCH INTERESTS
I'm interested in how the host circadian clock affects viral infection, at the molecular level in cells and also as disease develops in the whole animal. Reciprocally, I'm interested in how viruses can exploit our body clocks to aid their replication and spread.
Diverse biological processes exhibit circadian rhythms, including most facets of the immune response. In individual cells, molecular clocks coordinate a 24h programme of activity in fundamental processes such as gene transcription, translation, metabolism and bioenergetics. Using the model mouse pathogen Murid Herpesvirus 4, the circadian time of infection impacts upon virus replication in cells and disease progression in mice: Disease is enhanced when infection occurs at the onset of the rest period (morning), compared to infections occurring just prior to the activity (evening). Additionally, human pathogens e.g. Herpes Simplex Virus 1 and Influenza A cause more severe infection in mouse models where the circadian clock has been disrupted (arrhythmic Bmal1-/- mutants).
My work is focused on understanding the mechanistic basis of circadian clock/virus interactions, using infection at different times of day, in different 'clock mutants' and with different model viruses to dissect which clock-controlled processes exert influence over infection.
RESEARCH INTERESTS
I'm interested in how the host circadian clock affects viral infection, at the molecular level in cells and also as disease develops in the whole animal. Reciprocally, I'm interested in how viruses can exploit our body clocks to aid their replication and spread.
Diverse biological processes exhibit circadian rhythms, including most facets of the immune response. In individual cells, molecular clocks coordinate a 24h programme of activity in fundamental processes such as gene transcription, translation, metabolism and bioenergetics. Using the model mouse pathogen Murid Herpesvirus 4, the circadian time of infection impacts upon virus replication in cells and disease progression in mice: Disease is enhanced when infection occurs at the onset of the rest period (morning), compared to infections occurring just prior to the activity (evening). Additionally, human pathogens e.g. Herpes Simplex Virus 1 and Influenza A cause more severe infection in mouse models where the circadian clock has been disrupted (arrhythmic Bmal1-/- mutants).
My work is focused on understanding the mechanistic basis of circadian clock/virus interactions, using infection at different times of day, in different 'clock mutants' and with different model viruses to dissect which clock-controlled processes exert influence over infection.
研究兴趣
论文共 6 篇作者统计合作学者相似作者
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Joseph L Watson,Estere Seinkmane,Christine T Styles, Andrei Mihut, Lara K Krüger,Kerrie E McNally,Vicente Jose Planelles-Herrero, Michal Dudek,Patrick M McCall,Silvia Barbiero,Michael Vanden Oever,Sew Yeu Peak-Chew,
Christine T. Styles,Jie Zhou,Katie E. Flight,Jonathan C. Brown, Charlotte Lewis, Xinyu Wang,Michael Vanden Oever,Thomas P. Peacock,Ziyin Wang,Rosie Millns,John S. O'Neill, Alexander Borodavka,
EMBO MOLECULAR MEDICINEno. 12 (2023): e17932-e17932
medRxiv (2021)
medRxiv (Cold Spring Harbor Laboratory) (2021)
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Brain, behavior, and immunity (2019): 236-243
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