scholarly journals Identification of Functional Differences between Prototype Epstein–Barr Virus-Encoded LMP1 and a Nasopharyngeal Carcinoma-Derived LMP1 in Human Epithelial Cells

Virology ◽  
2000 ◽  
Vol 272 (1) ◽  
pp. 204-217 ◽  
Author(s):  
Christopher W. Dawson ◽  
Aristides G. Eliopoulos ◽  
Sarah M. Blake ◽  
Rachel Barker ◽  
Lawrence S. Young
Science ◽  
1983 ◽  
Vol 219 (4589) ◽  
pp. 1225-1228 ◽  
Author(s):  
I. Shapiro ◽  
D. Volsky

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.


2009 ◽  
Vol 11 (3) ◽  
pp. 429-433 ◽  
Author(s):  
Ken-Ichi Imadome ◽  
Norio Shimizu ◽  
Misako Yajima ◽  
Ken Watanabe ◽  
Hiroyuki Nakamura ◽  
...  

2009 ◽  
Vol 38 (6) ◽  
pp. 1932-1949 ◽  
Author(s):  
Chung-Chun Wu ◽  
Ming-Tsan Liu ◽  
Yu-Ting Chang ◽  
Chih-Yeu Fang ◽  
Sheng-Ping Chou ◽  
...  

1987 ◽  
Vol 90 (9) ◽  
pp. 1334-1338
Author(s):  
TORU TAKIMOTO ◽  
TAMEO MIYAZAKI ◽  
JUNICHI IWAWAKI ◽  
SHIGERU ISHIKAWA ◽  
SAICHIROH TANAKA ◽  
...  

Oncogene ◽  
1997 ◽  
Vol 15 (3) ◽  
pp. 275-283 ◽  
Author(s):  
L J Nicholson ◽  
P Hopwood ◽  
I Johannessen ◽  
J R Salisbury ◽  
J Codd ◽  
...  

2020 ◽  
Vol 2 (1) ◽  
pp. 113-120
Author(s):  
Nur Suci Amanah

Nasopharyngeal carcinoma is a common disease in southern China. The etiologies of the main factors proposed for the pathogenesis of KNF include genetic factors, environmental factors and Epstein Barr Virus (EBV) infection. Other causes besides preserved food consumption include salted fish which have been involved in the etiology of NPC. The downward trend in the incidence of NPC has occurred in Hong Kong for the past 20 years, which is caused by changes in dietary habits. Despite the close relationship of EBV infection with NPC, the etiological role of EBV in the pathogenesis of NPC remains an interaction. EBV infection in primary nasopharyngeal epithelial cells occurs. Epstein Barr virus does not convert primary nasopharyngeal epithelial cells into proliferative clones, which is in sharp contrast to the well-documented ability of EBV to alter and perpetuate primary B cells. Genetic changes that are supported in the nasopharyngeal epithelium may be needed to support stable EBV infection. Non-viral factors as a cause of nasopharyngeal carcinoma still cannot be resolved with certainty. Non-viral factors are one of the risk factors that can increase the number of events arising from nasopharyngeal malignancies such as smoke, salted fish, formaldehyde, genetic, as soon as possible firewood, wood dust, chronic infection, throat protector, alcohol and traditional medicine.


1992 ◽  
Vol 176 (5) ◽  
pp. 1405-1414 ◽  
Author(s):  
M Birkenbach ◽  
X Tong ◽  
L E Bradbury ◽  
T F Tedder ◽  
E Kieff

Epstein-Barr virus (EBV) adsorption to human B lymphocytes is mediated by the viral envelope glycoprotein, gp350/220, which binds to the cell surface protein, CD21, also known as the CR2 complement receptor. Human epithelial cells also express an EBV receptor. A candidate surface molecule of 195 kD has previously been identified on an epithelial cell line and explanted epithelial tissue by reactivity with the CD21 specific monoclonal antibody (mAb), HB-5a. In experiments to further characterize the epithelial cell EBV receptor, we have found that two human epithelial cell lines, RHEK-1 and HeLa, specifically bind intact EB virions. A 145-kD protein, similar in size to B lymphocyte CD21, was specifically precipitated from surface iodinated RHEK-1 cells using the HB-5a mAb, or using purified soluble gp350/220 coupled to agarose beads. The previously identified 195-kD protein did not bind to gp350/220 or react with two other anti-CD21 mAbs. CD21 homologous RNA, similar in size to the B lymphocyte CD21 mRNA, was detected in both RHEK-1 and HeLa cells. The nucleotide sequence of the epithelial cell cDNA was identical to B lymphocyte CD21. The longest clone differs from previously reported CD21 cDNAs in having additional 5' untranslated sequence. Polymerase chain reaction amplification of RHEK-1- or B lymphoblastoid-derived cDNA verified that most CD21 transcripts are initiated at least 30-50 nucleotides upstream of the previously reported mRNA cap site. These experiments demonstrate that human epithelial cells can express CD21, and that CD21 is likely to mediate EBV adsorption to epithelial cells.


Sign in / Sign up

Export Citation Format

Share Document