West Nile Virus replication and cellular stress responses
Professor Jason Mackenzie
+61 3 9035 8376
WNV dramatically alters the intracellular environment of infected cells. Earlier studies from our lab have shown that viral protein expression and assembly all occur at the endoplasmic reticulum (ER), and that this organelle is also a source of membranes for the replication structures observed during infection. As a result, WNV places a significant amount of stress on the ER, thus we are interested in investigating the effect that WNV replication has on the ER stress response. Our studies have shown that WNV modulates signalling from the ER to benefit replication, activating pro-survival pathways whilst simultaneously inhibiting pro-apoptotic and translational arrest effectors. We have also demonstrated that by hijacking this signalling pathway, WNV can concurrently inhibit antiviral signalling, and that this is mediated by the hydrophobic viral proteins. We are currently investigating the cross-talk between ER stress and anti-viral signalling, as well as determining the exact effectors of ER stress vital for WNV replication.
Figure 1: Our current model of how WNV can manipulate and modulate cellular responses to promote survival
Dr Rebecca Ambrose
Mackenzie laboratory: Intracellular virus replication and innate immunity
Faculty Research Themes
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Molecular Mechanisms of Disease
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