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Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis
Published on: April 17, 2017
Porcine deltacoronavirus infection promotes intracellular lipid droplet accumulation
Xiaohui Yang1, Haiwen Zhong1, Chuanzhao Yu2
1State Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou, 510642, China.
Background:
Viruses critically depend on host lipid metabolism to drive replication, assembly and immune evasion during infection and pathogenesis. While previous studies have demonstrated that certain viruses induce lipid droplet accumulation in infected host cells, lipid droplets have been reported to exert either proviral or antiviral effects across different research contexts. The present study investigates how porcine deltacoronavirus (PDCoV) regulates lipid droplet biogenesis and fatty acid synthesis in LLC-PK1 cells, with the aim of elucidating the potential molecular mechanisms and regulatory gene targets that govern lipid droplet homeostasis during infection.
Methods:
First, we characterized PDCoV's impact on lipid droplet homeostasis in LLC-PK1 cells using immunofluorescence staining, lipidomic profiling and gene expression analysis. Subsequently, we investigated the molecular mechanisms governing lipid droplets' antiviral effects against PDCoV, focusing on interferon (IFN) response pathway and endoplasmic reticulum (ER) stress signaling. Finally, we employed gene knockout (KO) strategy to study the regulatory gene of lipid metabolism that modulate the efficiency of PDCoV infection.
Results:
PDCoV infection caused significant accumulation of lipid droplets in LLC-PK1 cells. Transcriptional and lipidomic analyses revealed a disruption in lipid metabolism, characterized by altered gene expression and elevated cellular triacylglycerol (TAG) levels. Lipid droplets exhibited co-localization with actively replicating virus, suggesting a potential proviral role of lipid droplets in PDCoV infection. However, excessive lipid droplets accumulation strongly suppressed PDCoV infection. This antiviral effect was linked to enhanced type I/III IFN responses and ER stress. We further identified the pan-coronavirus host factor TMEM41B as a key regulator of lipid droplet homeostasis. TMEM41B KO induced aberrantly enlarged lipid droplets and potently inhibited PDCoV infection. Re-expression of TMEM41B restored both lipid droplet morphology and PDCoV infection, underscoring its role in modulating infection through lipid metabolic regulation.
Conclusions:
This work delineates host factors and mechanisms governing the lipid droplet-PDCoV interplay, revealing an antiviral strategy via chemical or genetic modulation of lipid droplet homeostasis.
