Intestinal epithelial cell surface glycans and associated receptors

Intestinal epithelial cell surface glycans and associated receptors constitute the multi-component machinery required for rotavirus attachment and internalization into host enterocytes. The infection process is initiated by the binding of the viral VP4 spike protein to specific glycans, primarily sialic acids or histo-blood group antigens (HBGAs) like H-type 1 and Lewis b, which serve as primary attachment factors [1][2]. Subsequent to this initial docking, the virus engages a series of proteinaceous co-receptors, including integrins alpha2beta1, alphavbeta3, and alphaXbeta2, as well as the heat shock cognate protein 70 (Hsc70), to trigger endocytic entry [3][4]. The expression patterns of these glycans, governed by host genetics such as the FUT2 (secretor) and FUT3 (Lewis) genes, are major determinants of individual susceptibility and strain-specific tropism [5]. Because these receptors are essential for the viral life cycle, they are prime targets for the development of entry inhibitors, including glycan mimetics and human milk oligosaccharides (HMOs) that competitively block viral binding [6].

Other names

Rotavirus entry receptorsHisto-blood group antigensHBGAsSialic acid receptorsIntegrin-Hsc70 entry complexVP4-binding glycans

Competitive inhibition of viral attachment to cell surface glycans and blocking of co-receptor mediated endocytosis.