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    Modulation of acyl-carnitines, the broad mechanism behind Wolbachia-mediated inhibition of medically important flaviviruses in Aedes aegypti

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    Author
    Manokaran, G; Flores, HA; Dickson, CT; Narayana, VK; Kanojia, K; Dayalan, S; Tull, D; McConville, MJ; Mackenzie, JM; Simmons, CP
    Date
    2020-09-29
    Source Title
    Proceedings of the National Academy of Sciences of USA
    Publisher
    NATL ACAD SCIENCES
    University of Melbourne Author/s
    McConville, Malcolm; Mackenzie, Jason; Narayana, Vinod; Simmons, Cameron
    Affiliation
    Biochemistry and Molecular Biology
    Melbourne School of Population and Global Health
    Microbiology and Immunology
    Bio21
    Metadata
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    Document Type
    Journal Article
    Citations
    Manokaran, G., Flores, H. A., Dickson, C. T., Narayana, V. K., Kanojia, K., Dayalan, S., Tull, D., McConville, M. J., Mackenzie, J. M. & Simmons, C. P. (2020). Modulation of acyl-carnitines, the broad mechanism behind Wolbachia-mediated inhibition of medically important flaviviruses in Aedes aegypti. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 117 (39), pp.24475-24483. https://doi.org/10.1073/pnas.1914814117.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251564
    DOI
    10.1073/pnas.1914814117
    Abstract
    Wolbachia-infected mosquitoes are refractory to flavivirus infections, but the role of lipids in Wolbachia-mediated virus blocking remains to be elucidated. Here, we use liquid chromatography mass spectrometry to provide a comprehensive picture of the lipidome of Aedes aegypti (Aag2) cells infected with Wolbachia only, either dengue or Zika virus only, and Wolbachia-infected Aag2 cells superinfected with either dengue or Zika virus. This approach identifies a class of lipids, acyl-carnitines, as being down-regulated during Wolbachia infection. Furthermore, treatment with an acyl-carnitine inhibitor assigns a crucial role for acyl-carnitines in the replication of dengue and Zika viruses. In contrast, depletion of acyl-carnitines increases Wolbachia density while addition of commercially available acyl-carnitines impairs Wolbachia production. Finally, we show an increase in flavivirus infection of Wolbachia-infected cells with the addition of acyl-carnitines. This study uncovers a previously unknown role for acyl-carnitines in this tripartite interaction that suggests an important and broad mechanism that underpins Wolbachia-mediated pathogen blocking.

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