期刊
CELL HOST & MICROBE
卷 24, 期 4, 页码 526-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2018.09.002
关键词
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资金
- Princeton University Microscopy and Mass Spectrometry Facilities
- NIH [GM114141]
- Mallinckrodt Scholar Award
- Harold W. Dodds Fellowship
- Princeton Centennial Fellowship
- NINS Strategic International Research Exchange Promotion Program
- National Science Foundation Graduate Research Fellowship [DGE-1656466]
- Burroughs Wellcome Collaborative Travel Grant
- Sy and Laurie Sternberg Award
Viral proteins have evolved to target cellular organelles and usurp their functions for virus replication. Despite the knowledge of these critical functions for several organelles, little is known about peroxisomes during infection. Peroxisomes are primarily metabolic organelles with important functions in lipid metabolism. Here, we discovered that the enveloped viruses human cytomegalovirus (HCMV) and herpes simplex virus type 1 (HSV-1) induce the biogenesis of and unique morphological changes to peroxisomes to support their replication. Targeted proteomic quantification revealed a global virus-induced upregulation of peroxisomal proteins. Mathematical modeling and microscopy structural analysis show that infection triggers peroxisome growth and fission, leading to increased peroxisome numbers and irregular disc-like structures. HCMV-induced peroxisome biogenesis increased the phospholipid plasmalogen, thereby enhancing virus production. Peroxisome regulation and dependence were not observed for the non-enveloped adenovirus. Our findings uncover a role of peroxisomes in viral pathogenesis, with likely implications for multiple enveloped viruses.
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