Lipid Droplet Motility Increases Following Viral Immune Stimulation

Abstract

Lipid droplets (LDs) have traditionally been thought of as solely lipid storage compartments for cells; however, in the last decade, they have emerged as critical organelles in health and disease. LDs are highly dynamic within cells, and their movement is critical in organelle–organelle interactions. Their dynamics are known to change during cellular stress or nutrient deprivation; however, their movement during pathogen infections, especially at very early timepoints, is under-researched. This study aimed to track LD dynamics in vitro, in an astrocytic model of infection. Cells were either stimulated with a dsRNA viral mimic, poly I:C, or infected with the RNA virus, Zika virus. Individual LDs within infected cells were analysed to determine displacement and speed, and average LD characteristics for multiple individual cells calculated. Both LD displacement and mean speed were significantly enhanced in stimulated cells over a time course of infection with an increase seen as early as 2 h post-infection. With the emerging role for LDs during innate host responses, understanding their dynamics is critical to elucidate how these organelles influence the outcome of viral infection.

Lipid droplets in the nervous system

“…Lipid droplets play a fundamental role in the host–pathogen relationship, as evidenced by the rapid increase in lipid droplet numbers following infection with virus ( Samsa et al, 2009 ; Monson et al, 2021 ), bacteria ( D’Avila et al, 2006 ; Kumar et al, 2006 ), fungi ( Sorgi et al, 2009 ), and protozoa ( Vallochi et al, 2018 ; Melo et al, 2003 ; D’Avila et al, 2011 ; Rodríguez et al, 2017 ). The life cycle of many viruses is intimately tied to the host’s lipid metabolism ( Thomssen et al, 1992 ; Herker and Ott, 2012 ).…”

Lipid Droplets and Their Participation in Zika Virus Infection

“…In the model of infected astrocytes, cells were infected with ZIKV or stimulated with poly I:C, a dsRNA virus mimic. The LD displacement and average velocity in cells were significantly enhanced 2 h after infection or stimulation, indicating that the dynamics of LDs had changed in the early stage of pathogen infection, further supporting the emerging role of LDs in the innate host response [ 143 ]. Another study showed that hydroxysteroid (17β) dehydrogenase (HSD17B)12 promotes the replication of ZIKV and the production of infectious particles by increasing LD biosynthesis, which plays a key role in virus assembly.…”

The interplay between lipid droplets and virus infection

“…Like DENV, Zika virus (ZIKV) infection alters LD number as well as its mobility. 121 Qin et al showed that ZIKV infection also induces lipophagy by activating AMPK-ULK1 signaling in human hepatoma cells. 122 In placental cells, ZIKV modulates LDs in both infected and bystander cells and LD formation is required for ZIKV replication.…”

“…Like DENV, Zika virus (ZIKV) infection alters LD number as well as its mobility 121 . Qin et al showed that ZIKV infection also induces lipophagy by activating AMPK‐ULK1 signaling in human hepatoma cells 122 .…”