Key result
Adenovirus type 5 rapidly increases paracellular permeability and alters E-cadherin dynamics via CAR modulation.
Why the study?
The mechanism by which Adenovirus type 5 disrupts cell junctions and facilitates virus escape via CAR and E-cadherin dynamics was not fully understood.
Ad5 increases paracellular permeability early after infection by altering E-cadherin dynamics, potentially facilitating virus access to receptors.
Should not alter adenovirus vector protocols; leaves open whether junctional effects enhance dissemination in epithelial tissues.
Adenovirus (Ad) serotype 5 (Ad5) fiber competitively binds to the coxsackievirus and Ad receptor (CAR) to attach Ad5 to target cells and also disrupts cell junctions and facilitates virus escape at a late stage in Ad5 infection. Here we demonstrate that paracellular permeability in MCF7 and CAR overexpressing MCF7 (FLCARMCF7) cells is increased within minutes following the addition of Ad5 to cells. This is brought about, at least in part, by altering the molecular dynamics of E-cadherin, a key component of the cell-cell adhesion complex. We also demonstrate that the increase in E-cadherin mobility is constitutively altered by the presence of CAR at FLCARMCF7 cell junctions. As increased paracellular permeability was observed early after the addition of Ad5 to cells, we postulate that this may represent a mechanism by which Ad5 could disrupt cell junctions to facilitate further access to its cell receptors.
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Hussain et al. (2011) studied Adenovirus infection (in vitro). Adenovirus Type 5 (Ad5eGFP) vs. No Ad5eGFP was evaluated on Paracellular permeability and E-cadherin mobility. Adenovirus Type 5 rapidly increases paracellular permeability and alters E-cadherin molecular dynamics in MCF7 cells, an effect modulated by the presence of the coxsackievirus and adenovirus receptor (CAR).
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