Implications for lipids during replication of enveloped viruses

Abstract

Enveloped viruses, which include many medically important viruses such as human immunodeficiency virus, influenza virus and hepatitis C virus, are intracellular parasites that acquire lipid envelopes from their host cells. Success of replication is intimately linked to their ability to hijack host cell mechanisms, particularly those related to membrane dynamics and lipid metabolism. Despite recent progress, our knowledge of lipid mediated virus-host interactions remains highly incomplete. In addition, diverse experimental systems are used to study different stages of virus replication thus complicating comparisons. This review aims to present a unifying view of the widely diverse strategies used by enveloped viruses at distinct stages of their replication cycles.

Fig. 1

(A) Overview of lipid classes discussed in this review: cholesterol (Chol), ceramide (Cer), sphingomyelin (SM), ganglioside GM3 (GM3), phosphatidylinositol-4,5-bis-phosphate (PI(4,5)P₂), plasmalogen phosphatidylethanolamine (pPE), phosphatidylserine (PS) and cardiolipin (CL); (B) lipid-bilayer arrangement during virus budding: lipid species are coloured according to their head group as described in (A). Lipids are asymmetrically distributed in the plasma membrane and virus budding occurs at sites enriched in cholesterol, sphingolipids and phosphoinositides. Yellow arrows indicate the targeting of proteins to the plasma membrane through electrostatic interaction with phosphoinositides. This results in a pushing-force finally leading to virus budding. (C) Lipid distribution in the virus envelope: enrichment of sphingolipids and cholesterol in the lipid envelope bestows fluidity and stability to the virus. Such and other lipids have also an important role in virus entry.