Epstein‐Barr virus envelope glycoprotein gp350 induces NF‐κB activation and IL‐1β synthesis in human monocytes‐macrophages involving PKC and PI3‐K

1999 ◽  
Vol 13 (15) ◽  
pp. 2203-2213 ◽  
Author(s):  
M. D'ADDARIO ◽  
A. AHMAD ◽  
J. W. XU ◽  
J. MENEZES
2006 ◽  
Vol 194 (5) ◽  
pp. 584-587 ◽  
Author(s):  
Tanzina Haque ◽  
Ingolfur Johannessen ◽  
Dilani Dombagoda ◽  
Chandrya Sengupta ◽  
David M. Burns ◽  
...  

2006 ◽  
Vol 80 (19) ◽  
pp. 9628-9633 ◽  
Author(s):  
Susan M. Turk ◽  
Ru Jiang ◽  
Liudmila S. Chesnokova ◽  
Lindsey M. Hutt-Fletcher

ABSTRACT Epstein-Barr virus (EBV) is a persistent, orally transmitted herpesvirus that replicates in B cells and epithelial cells and is associated with lymphoid and epithelial malignancies. The virus binds to CD21 on B cells via glycoprotein gp350/220 and infects efficiently. Infection of cultured epithelial cells has not typically been efficient but can occur in the absence of gp350/220 and CD21 and in vivo is thought to be important to the development of nasopharyngeal carcinoma. We report here that antibodies to gp350/220, which inhibit EBV infection of B cells, enhance infection of epithelial cells. The effect is not mediated by Fc receptor binding but is further enhanced by antibody cross-linking, which may patch gp350/220 in the virus envelope. Saliva from EBV-seropositive individuals has similar effects that can be reversed by depletion of antibody. The results are consistent with a model in which gp350/220 interferes with the access of other important players to the epithelial cell surface. The results may have implications for the development of nasopharyngeal carcinoma in high-risk populations in which elevated titers of antibody to EBV lytic cycle proteins are prognostic.


Gene ◽  
1987 ◽  
Vol 54 (1) ◽  
pp. 113-123 ◽  
Author(s):  
Loren D. Schultz ◽  
Jerry Tanner ◽  
Kathryn J. Hofmann ◽  
Emilio A. Emini ◽  
Jon H. Condra ◽  
...  

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