Fig. 7
From: Metabolic reprogramming and lipid droplets are involved in Zika virus replication in neural cells
Conclusion. ZIKV is able to modulate the expression of important genes in lipid metabolism pathways, leading to increased levels of PPAR-γ and activation of SREBP-1. ZIKV infection increases the expression of FASN, which plays a role in fatty acid synthesis and is regulated by PPAR-γ. In addition, ZIKV decreases the levels of ATGL and HSL, important lipolytic enzymes. Therefore, these lipid metabolism regulations possibly contribute to the increase in LDs observed during ZIKV infection, and the biogenesis of this organelle is dependent on the DGAT-1 enzyme during infections. Treatment with the pharmacological inhibitor of DGAT-1, A922500, reduces the biogenesis of LDs and reduces the replication of ZIKV, contributing to the decrease in the production of inflammatory mediators. Altogether, our data suggest that LDs are important for the replication of ZIKV, participating in ZIKV pathogenesis