Norovirus binding to intestinal epithelial cells is independent of histo-blood group antigens

PLoS One. 2013 Jun 14;8(6):e66534. doi: 10.1371/journal.pone.0066534. Print 2013.

Abstract

Human noroviruses (NoVs) are a major cause of non-bacterial gastroenteritis. Although histo-blood group antigens (HBGAs) have been implicated in the initial binding of NoV, the mechanism of that binding before internalization is not clear. To determine the involvement of NoVs and HBGAs in cell binding, we examined the localization of NoV virus-like particles (VLPs) and HBGAs in a human intestinal cell line and the human ileum biopsy specimens by immunofluorescence microscopy. The localizations of Ueno 7k VLPs (genogroup II.6) and each HBGA (type H1-, H2- and Le(b)-HBGAs) on the human intestinal cell line, Caco-2, were examined by confocal laser-scanning microscopy. To explore any interactions of NoVs and HBGAs in vivo, fresh biopsy specimens from human ileum were directly incubated with NoV VLPs and examined by immunofluorescence microscopy. We found that VLP binding depended on the state of cell differentiation, but not on the presence of HBGAs. In differentiated Caco-2 cells, we detected no type H1 HBGAs, but VLPs bound to the cells anyway. We incubated fresh biopsies of human ileum directly with VLPs, a model that better replicates the in vivo environment. VLPs mainly bound epithelial cells and goblet cells. Although the incubations were performed at 4°C to hinder internalization, VLPs were still detected inside cells. Our results suggest that VLPs utilize molecule(s) other than HBGAs during binding and internalization into cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Group Antigens / metabolism*
  • Caco-2 Cells
  • Cell Differentiation
  • Epithelial Cells / metabolism
  • Epithelial Cells / virology*
  • Host-Pathogen Interactions
  • Humans
  • Intestinal Mucosa / cytology*
  • Norovirus / physiology*
  • Virion / physiology
  • Virus Attachment*

Substances

  • Blood Group Antigens

Grants and funding

This work was supported by Grants-in-Aid for Scientific Research from Japan Society for the Promotion of Science (JSPS KAKENHI Grand numbers 20380184, 24380069 and 23590556, http://www.jsps.go.jp/english/e-grants/index.html), by Grants-in-Aid from the Ministry of Health, Labor and Welfare of Japan (Research on Emerging and Re-emerging Infectious Diseases Grand numbers 11103251 and 12103310, http://www.mhlw.go.jp/english/policy/other/research-projects/index.html). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.