Abstract
Sphingolipids are essential components of eukaryotic cells. In this review, we want to exemplarily illustrate what is known about the interactions of sphingolipids with various viruses at different steps of their replication cycles. This includes structural interactions during entry at the plasma membrane or endosomal membranes, early interactions leading to sphingolipid-mediated signal transduction, interactions with internal membranes and lipids during replication, and interactions during virus assembly and budding. Targeted interventions in sphingolipid metabolism – as far as they can be tolerated by cells and organisms – may open novel possibilities to support antiviral therapies. Human immunodeficiency virus type 1 (HIV-1) infections have intensively been studied, but for other viral infections, such as influenza A virus (IAV), measles virus (MV), hepatitis C virus (HCV), dengue virus, Ebola virus, and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), investigations are still in their beginnings. As many inhibitors of sphingolipid metabolism are already in clinical use against other diseases, repurposing studies for applications in some viral infections appear to be a promising approach.
Highlights
As obligate intracellular pathogens, viruses must interact with and overcome cellular membranes as a key step of their life cycle
As dendritic cells function as cellular ferries of measles virus (MV), this may be important for transmitting MV during viral exit from the infected individual (Derakhshani et al, 2019). These findings show that predominantly ceramide and S1P are important signaling molecules regulating the cell metabolism, but which are intrinsically tied to the capacity of a target cell to replicate viruses
Many chemical compounds affecting sphingolipid metabolism have been tested in animal models in vivo or are already in clinical use against diseases as divers as cancer and multiple sclerosis
Summary
Viruses must interact with and overcome cellular membranes as a key step of their life cycle. This includes structural interactions during entry at the plasma membrane or endosomal membranes, early interactions leading to sphingolipid-mediated signal transduction, interactions with internal membranes and lipids during replication, and interactions during virus assembly and budding.
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