Published online May 12, 2016. doi: 10.5501/wjv.v5.i2.38
Peer-review started: August 13, 2015
First decision: September 28, 2015
Revised: December 2, 2015
Accepted: January 27, 2016
Article in press: January 29, 2016
Published online: May 12, 2016
Core tip: Rotavirus entry into the host cell requires cell surface molecules providing binding, chaperoning and oxido-reducing functions. Sialic acid/integrin α2β1, heat shock cognate protein 70 and protein disulfide isomerase (PDI) seem to perform these functions. Recently, the cell surface oxido-reduction activity based at least on PDI has been highlighted as a potential determinant of the conformational changes that are required by viral structural proteins in order to facilitate virus entry. The rotavirus-induced oxidative stress and inflammatory signaling is an attractive target for therapeutic intervention as antioxidant and anti-inflammatory treatment has proved to efficiently inhibit rotavirus infection.