Abstract
Diseases caused by Flaviviridae have a wide global and economic impact due to high morbidity and mortality. Flaviviridae infection usually leads to severe, acute or chronic diseases, such as liver injury and liver cancer resulting from hepatitis C virus (HCV) infection, dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS) caused by dengue virus (DENV). Given the highly complex pathogenesis of Flaviviridae infections, they are still not fully understood at present. Accumulating evidence suggests that host autophagy is disrupted to regulate the life cycle of Flaviviridae. Organelle-specific autophagy is able to selectively target different organelles for quality control, which is essential for regulating cellular homeostasis. As an important sub process of autophagy, lipophagy regulates lipid metabolism by targeting lipid droplets (LDs) and is also closely related to the infection of a variety of pathogenic microorganisms. In this review, we briefly understand the LDs interaction relationship with Flaviviridae infection, outline the molecular events of how lipophagy occurs and the related research progress on the regulatory mechanisms of lipophagy in Flaviviridae infection. Exploring the crosstalk between viral infection and lipophagy induced molecular events may provide new avenues for antiviral therapy.
Highlights
Viruses, as highly parasitic microorganisms, have to rely entirely on the host cell processes to complete their life cycle due to the lack of essential metabolic machinery required for replication or assembly
A follow-up study revealed that PLIN 2, the substrate of chaperone mediated autophagy (CMA), forms p-PLIN 2 by phosphorylation (P) through AMP-activated protein kinase (AMPK) and translocation from the lipid droplets (LDs) surface to lysosomes, where it promotes the recruitment of a neutral lipid lipase (ATGL) and macrolipophagy machinery components to the LD (Kaushik and Cuervo, 2016)
This study found that dengue virus (DENV) infection of hepatocytes quickly increases the number of autophagosomes associated with LDs and transfers them to lysosomes for degradation (Jordan and Randall, 2017)
Summary
As highly parasitic microorganisms, have to rely entirely on the host cell processes to complete their life cycle due to the lack of essential metabolic machinery required for replication or assembly. Recent studies show that the LDs-associated proteins Rab18 and Rab1A interact with CSFV NS5A protein, an essential replicase component, which have been shown to mediate viral replication and assembly process (Lin et al, 2018; Zhang et al, 2020).
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