Abstract
Lipids and pathogenic flaviviruses: An intimate union.
Highlights
The viral replication cycle presents viruses with a series of logistical challenges: To be successful, the virus must synthesize new copies of its genetic material, induce the cell to translate its genome into protein, and coordinate the host and viral factors required to assemble new virus particles
The emergence and expansion of Zika virus (ZIKV) and other flaviviruses into new populations, and association with novel pathologies like microcephaly, have lent urgency to efforts to understand the host–virus interactions leading to disease, many of which remain enigmatic
Lipidomic analyses of cells infected with flaviviruses have shown that viral replication triggers significant changes in global lipid profiles, suggesting similar mechanisms may be required for viral membrane remodeling [19,20,21,22]
Summary
The viral replication cycle presents viruses with a series of logistical challenges: To be successful, the virus must synthesize new copies of its genetic material, induce the cell to translate its genome into protein, and coordinate the host and viral factors required to assemble new virus particles. Much of this occurs at intracellular membranes, and lipid bilayers are expected to both play a central role in organizing the molecular machinery required for each stage of virion biogenesis and provide a structural foundation for particle assembly. While the architectural features of RC membranes have been extensively studied, the emerging discipline of lipidomics has yielded new insight into the ways in which positive-strand RNA viruses modulate host lipid metabolism to create lipid environments favorable to RC formation and viral replication
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