Fig 1.
Microscopy images of ZIKV-infected HeLa Cells 24 hours after infection.
(A) Electron micrograph of ER-derived vacuoles in a ZIKV-infected cell. (B) Confocal microscopy image showing the colocalization (yellow/orange) of ER-shaping protein ATL3 (green) with the ZIKV protein NS3 (red). ATL3, Atlastin-3; ER, endoplasmic reticulum; NS3, nonstructural protein 3; ZIKV, Zika virus.
Fig 2.
The relationship between ER-shaping proteins and flaviviruses during infection.
A simplified schematic showing the interaction between different flavivirus proteins and ER-shaping proteins: (A) RTN3.1A and (B) ATL2 (left) and ATL3 (right). (C) Depleting RTN3.1 results in elongated RCs in DENV-infected cells and fewer RCs per VP in WNV-infected and ZIKV-infected cells. (D) Depleting ATL2 (left) results in VPs that are smaller, distorted, and condensed but does not change the overall number of VPs, whereas ATL3 depletion results in the host-protease Furin relocating from the perinuclear region to the cell periphery and accumulation of immature virus particles in the ER lumen. Immature virus particles are represented smaller than they would be in relation to VPs. ATL2, Atlastin-2; ATL3, Atlastin-3; DENV, dengue virus; ENV, envelope; ER, endoplasmic reticulum; NS1, nonstructural protein 1; RC, replication complex; RTN3.1A, Reticulon 3.1A; VP, vesicle packet; WNV, West Nile virus; ZIKV, Zika virus.