Lipid membranes in poxvirus replication

Abstract

Poxviruses replicate in the cytoplasm, where they acquire multiple lipoprotein membranes. Although a proposal that the initial membrane arises de novo has not been substantiated, there is no accepted explanation for its formation from cellular membranes. A subsequent membrane-wrapping step involving modified trans-Golgi or endosomal cisternae results in a particle with three membranes. These wrapped virions traverse the cytoplasm on microtubules; the outermost membrane is lost during exocytosis, the middle one is lost just prior to cell entry, and the remaining membrane fuses with the cell to allow the virus core to enter the cytoplasm and initiate a new infection.

Keywords: endocytosis; exocytosis; phospholipids; transmembrane proteins; virus assembly; virus entry.

Figure 1.

Cell entry pathways of vaccinia virus mature virions (MV) and enveloped virions (EV) following attachment at the cell plasma membrane. Depending on the VACV strain and target cell, MV cores can enter the cytosol either through direct fusion of the MV membrane with the plasma membrane (A) or, following endocytosis/macropinocytosis, through fusion of the MV membrane with vesicles (B). EV particles have been observed to shed their additional membrane bilayer prior to direct fusion of the underlying MV membrane with the cell plasma membrane (C); entry of EV through an endosomal route might also occur. White arrowheads denote sites of membrane fusion between the MV particle membrane and cellular membranes.

Figure 2.

Enumeration of lipid membrane bilayers (white arrowhead) possessed by vaccinia virus assembly intermediates. Nucleoids (nu) are electron-dense, DNA-containing substructures of immature virions. Lateral bodies (L) are internal virion structures of heterogenous material surrounding the dumbbell-shaped viral core (C). The location of each morphogenic form is indicated below the respective schematic.