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@plosbiology.orgSep 17, 2026, 4:30 PM

#Flaviviruses reshape cell membranes to build replication sites, but how are these organized? This study shows that homotypic #membrane tethering driven by host ER protein atlastin-2 is essential for organizing these sites & supporting #viral replication @plosbiology.org 🧪 buff.ly/9MBKCbR

Left: A549 cells expressing HA-tagged ATL2 were infected with ZIKV. After 48 h, cells were fixed with paraformaldehyde and glutaraldehyde, followed by staining for dsRNA and HA using specific antibodies and reversible saponin permeabilization. Cells were imaged by confocal microscopy, then immediately embedded and processed for EM imaging. Right: Model. ATL2 membrane tethering is critical for the spatial organization of flavivirus genome replication. ATL2 tethering dimers bring ER membranes into close contact, facilitating the trafficking of newly synthesized viral genomes from existing vROs into vROs forming on juxtaposed membranes (top). This close connection forms a microdomain which brings together the necessary factors for nascent vRO formation and shields the cytosol-exposed viral RNA from innate immune sensors. Because membrane tethering is reversible, this also permits the expansion of viral genome replication away from sites of existing vRO biogenesis. In the absence of ATL2 membrane tethering (bottom), viral genomes extruded from the vRO are exposed to the cytosol and more likely to form new vROs on the same membrane, leading to the concentration of sites of vRO biogenesis and increased recognition by RIG-I-like receptors (RLRs) in the cytosol.
@plosbiology.orgSep 16, 2026, 1:05 PM

#Flaviviruses reshape cell membranes to build replication sites, but how are these organized? This study shows that homotypic #membrane tethering driven by host ER protein atlastin-2 is essential for organizing these sites & supporting #viral replication @plosbiology.org 🧪 buff.ly/9MBKCbR

Left: A549 cells expressing HA-tagged ATL2 were infected with ZIKV. After 48 h, cells were fixed with paraformaldehyde and glutaraldehyde, followed by staining for dsRNA and HA using specific antibodies and reversible saponin permeabilization. Cells were imaged by confocal microscopy, then immediately embedded and processed for EM imaging. Right: Model. ATL2 membrane tethering is critical for the spatial organization of flavivirus genome replication. ATL2 tethering dimers bring ER membranes into close contact, facilitating the trafficking of newly synthesized viral genomes from existing vROs into vROs forming on juxtaposed membranes (top). This close connection forms a microdomain which brings together the necessary factors for nascent vRO formation and shields the cytosol-exposed viral RNA from innate immune sensors. Because membrane tethering is reversible, this also permits the expansion of viral genome replication away from sites of existing vRO biogenesis. In the absence of ATL2 membrane tethering (bottom), viral genomes extruded from the vRO are exposed to the cytosol and more likely to form new vROs on the same membrane, leading to the concentration of sites of vRO biogenesis and increased recognition by RIG-I-like receptors (RLRs) in the cytosol.
@plosbiology.orgSep 16, 2026, 8:43 AM

#Flaviviruses reshape cell membranes to build replication sites, but how are these organized? This study shows that homotypic #membrane tethering driven by host ER protein atlastin-2 is essential for organizing these sites & supporting #viral replication @plosbiology.org 🧪 plos.io/3VxdbxK

Left: A549 cells expressing HA-tagged ATL2 were infected with ZIKV. After 48 h, cells were fixed with paraformaldehyde and glutaraldehyde, followed by staining for dsRNA and HA using specific antibodies and reversible saponin permeabilization. Cells were imaged by confocal microscopy, then immediately embedded and processed for EM imaging. Right: Model. ATL2 membrane tethering is critical for the spatial organization of flavivirus genome replication. ATL2 tethering dimers bring ER membranes into close contact, facilitating the trafficking of newly synthesized viral genomes from existing vROs into vROs forming on juxtaposed membranes (top). This close connection forms a microdomain which brings together the necessary factors for nascent vRO formation and shields the cytosol-exposed viral RNA from innate immune sensors. Because membrane tethering is reversible, this also permits the expansion of viral genome replication away from sites of existing vRO biogenesis. In the absence of ATL2 membrane tethering (bottom), viral genomes extruded from the vRO are exposed to the cytosol and more likely to form new vROs on the same membrane, leading to the concentration of sites of vRO biogenesis and increased recognition by RIG-I-like receptors (RLRs) in the cytosol.