THE MECHANISM OF EPSTEIN-BARR-VIRUS INFECTION IN NASOPHARYNGEAL CARCINOMA-CELLS

To investigate the relationship between Epstein-Barr virus (EBV) and n asopharyngeal carcinoma (NPC) cells, we examined the pathway of EBV in fection in NPC cell lines. We used immunolocalization to investigate t he EBV receptor (C3d-R) and polymeric immunoglobulin receptor [secreto ry component (SC) protein]. We incubated IgA anti-EBV and EBV particle s with NPC cells and observed the EBV DNA signal by in situ polymerase chain reaction hybridization and polymerase chain reaction plus South ern blotting. We also colocalized SC protein and EBV RNA in NPC cells did not express the EBV receptor but did express SC protein in each li ne; 2) SC protein was also expressed in some tumor cells but not in un transformed squamous metaplastic epithelia in NPC biopsy specimens; 3) EBV could infect NPC cells through and EBV-IgA and SC complex and ret ained an EBV viral genome in their nuclei; SC expression could be down -regulated by EBV proteins; and 4) in biopsy specimens, a fraction of tumor cells showed SC protein expression; only a portion of tumor cell s contained EBV, and of these cells only a few expressed SC protein. T hese findings indicate that EBV cannot infect untransformed nasopharyn geal squamous metaplastic epithelia but can enter NPC cells through Ig A-mediated endocytosis.