| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2473180 | Current Opinion in Virology | 2016 | 5 Pages |
•Rotavirus viroplasms and lipid droplets associate early during viral replication.•Lipid droplets may act as a platform for viral replication and assembly.•Inhibition or disruption of lipid droplets reduces rotavirus yield.•Rotavirus-infected mice shed less virus upon lipid depletion.•Lipid droplet-disrupting compounds may be developed to combat LD-requiring pathogens.
Recent evidence has demonstrated that a variety of pathogens target cellular lipid metabolism for their replication. Lipid droplets are a major contributor to lipid homeostasis and contain neutral fats but are also recognized as dynamic organelles involved in signal transduction, membrane trafficking and modulation of immune and inflammatory responses. Rotaviruses co-opt lipid droplets for their replication. Rotavirus viroplasms, sites of viral RNA replication and immature particle assembly, form complexes with cellular lipid droplets early in infection. Chemical compounds blocking fatty acid synthesis or interfering with lipid droplet homeostasis decrease viroplasm formation and the yield of infectious viral progeny. Lipid droplets are vital for the replication of rotaviruses as well as various members of the Flaviviridae family and several intracellular bacteria. Chemical compounds decreasing intracellular triglyceride content reduced rotavirus replication in an animal model and should be considered as potential therapeutic agents against disease caused by rotaviruses, flaviviruses and intracellular bacteria.
