Selected article for: "cell glycosylation and viral infection"

Author: CHARLEY, B.; LAVENANT, L.; DELMAS, B.
Title: Glycosylation is Required for Coronavirus TGEV to Induce an Efficient Production of IFNα by Blood Mononuclear Cells
  • Cord-id: 5szalmsz
  • Document date: 2006_6_29
  • ID: 5szalmsz
    Snippet: Porcine peripheral blood mononuclear cells (PBMC) are induced to produce interferon alpha (IFNα) following in vitro exposure to coronavirus TGEV (transmissible gastroenteritis virus)‐infected glutaraldehyde‐fixed cell monolayers or lo TGEV virions. In the present report, we examined the possibility that glycosylation of viral proteins could play a major role in interactions with PBMC leading to the production of IFNα. Con A pretreatment of TGEV‐infected cell monolayers before fixation wi
    Document: Porcine peripheral blood mononuclear cells (PBMC) are induced to produce interferon alpha (IFNα) following in vitro exposure to coronavirus TGEV (transmissible gastroenteritis virus)‐infected glutaraldehyde‐fixed cell monolayers or lo TGEV virions. In the present report, we examined the possibility that glycosylation of viral proteins could play a major role in interactions with PBMC leading to the production of IFNα. Con A pretreatment of TGEV‐infected cell monolayers before fixation with glutaraldehyde and exposure to PBMC caused a dose‐dependent inhibition of IFNα induction, implying that masking of carbohydrates at the surface of infected cells lowered IFNα induction. Similarly, inhibition of N‐linked glycosylation by tunicamycin during viral infection of cell monolayers altered their ability to induce IFNα. In addition, complete cleavage of complex type' oligosaccharides by peptide‐N‐glycohydrolase Flowered the capacity of TGEV virions to induce IFNα. Thus, these findings strongly suggest that glycosylation of the viral proteins, and more precisely the presence of complex‐type oligosaccharides, is an important requirement for a completely efficient interaction with PBMC leading to the production of IFN‐α.

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