Author response image 2. Schematic representation of hypothesised mechanism of tight junction barrier damage under hyperglycaemic conditions in vitro.

Active replicating virus triggers signalling either directly or indirectly acting on the endothelial cells (1). Endothelial cells exposed to a history of hyperglycaemia produce a heat-labile soluble protein into the supernatant (3). This soluble factor acts upon the tight junction proteins of the epithelial cells, causing degradation and barrier permeability in both infected and non-infected epithelial cells (4). Image created with Biorender.