Correction: Chromosome Site for Epstein-Barr Virus DNA in a Burkitt Tumor Cell Line and in Lymphocytes Growth-transformed in vitro

1983 ◽  
Vol 80 (14) ◽  
pp. 4559-4559
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Tumor Cell Line ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals An Epstein-Barr Virus Isolated from a Lymphoblastoid Cell Line Has a 16-Kilobase-Pair Deletion Which Includes gp350 and the Epstein-Barr Virus Nuclear Antigen 3A

2001 ◽  
Vol 75 (18) ◽  
pp. 8556-8568 ◽  
Author(s):  
Wonkeun Lee ◽  
Yoon-Ha Hwang ◽  
Suk-Kyeong Lee ◽  
Chitra Subramanian ◽  
Erle S. Robertson
Keyword(s):  
Cell Line ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Phorbol Esters ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Amino Terminal ◽  
Epstein Barr

ABSTRACT Epstein-Barr virus (EBV) is associated with human cancers, including nasopharyngeal carcinoma, Burkitt's lymphoma, gastric carcinoma and, somewhat controversially, breast carcinoma. EBV infects and efficiently transforms human primary B lymphocytes in vitro. A number of EBV-encoded genes are critical for EBV-mediated transformation of human B lymphocytes. In this study we show that an EBV-infected lymphoblastoid cell line obtained from the spontaneous outgrowth of B cells from a leukemia patient contains a deletion, which involves a region of approximately 16 kbp. This deletion encodes major EBV genes involved in both infection and transformation of human primary B lymphocytes and includes the glycoprotein gp350, the entire open reading frame of EBNA3A, and the amino-terminal region of EBNA3B. A fusion protein created by this deletion, which lies between the BMRF1 early antigen and the EBNA3B latent antigen, is truncated immediately downstream of the junction 21 amino acids into the region of the EBNA3B sequence, which is out of frame with respect to the EBNA3B protein sequence, and indicates that EBNA3B is not expressed. The fusion is from EBV coordinate 80299 within the BMRF1 sequence to coordinate 90998 in the EBNA3B sequence. Additionally, we have shown that there is no detectable induction in viral replication observed when SNU-265 is treated with phorbol esters, and no transformants were detected when supernatant is used to infect primary B lymphocytes after 8 weeks in culture. Therefore, we have identified an EBV genome with a major deletion in critical genes involved in mediating EBV infection and the transformation of human primary B lymphocytes that is incompetent for replication of this naturally occurring EBV isolate.

scholarly journals In vitro Studies and Clinical Observations Imply a Synergistic Effect Between Epstein-Barr Virus and Dengue Virus Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiao-Mei Deng ◽  
Ling-Zhai Zhao ◽  
Xue-Ying Liang ◽  
Dan Li ◽  
Lei Yu ◽  
...  
Keyword(s):  
Synergistic Effect ◽  
Dengue Virus ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Severe Dengue ◽  
Complex Spectrum ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Dengue virus (DENV) infection can lead to a complex spectrum of clinical outcomes, ranging from asymptomatic infection to life-threatening severe dengue. The reasons for thus drastically varying manifestations of the disease remain an enigma. Herein, we reported an original discovery of the synergistic effect between preexisting Epstein–Barr virus (EBV) infection and DENV superinfection in vitro and of a strong correlation of these two viruses in the clinical samples from dengue patients. We showed that (I) DENV-2 infection of an EBV-positive cell line (EBV + Akata cell) reactivated EBV, and it could be blocked by wortmannin treatment. (II) Examination of human peripheral blood mononuclear cell (PBMC) samples from dengue patients revealed significantly elevated cell-associated EBV DNA copy number at the time of hospitalization vs. at the time of disease recovery in most individuals. (III) EBV infection promoted DENV propagation in both EBV-hosting B cells and indirectly in THP-1 cells, supported by the following evidence: (A) EBV + Akata cells were more permissive to DENV-2 infection compared with Akata cells harboring no EBV virus (EBV- Akata cells). (B) Low-molecular weight fraction secreted from EBV + Akata cells could enhance DENV-2 propagation in monocytic THP-1 cells. (C) While reactivation of EBV in EBV + Akata cells further increased DENV-2 yield from this cell line, pharmacological inhibition of EBV replication by acyclovir had the opposite effect. To our knowledge, this is the first investigation demonstrating a positive correlation between EBV and DENV in vitro and in human biospecimens.

scholarly journals Helper cell-independent cytotoxic clones in man.

1982 ◽  
Vol 156 (6) ◽  
pp. 1854-1859 ◽  
Author(s):  
S L Wee ◽  
L K Chen ◽  
G Strassmann ◽  
F H Bach
Keyword(s):  
T Cell ◽  
Epstein Barr Virus ◽  
Helper Cell ◽  
Cytotoxic T Cell ◽  
Lymphoblastoid Cell Lines ◽  
Barr Virus ◽  
Mediate Cytotoxicity ◽  
Epstein Barr ◽  
And Function

We report here a class of helper cell-independent cytotoxic T cell (HITc) clones in man that can proliferate in response to antigenic stimulation as well as mediate cytotoxicity. HITc appear to be rare among clones derived from primary in vitro allosensitized culture, but constitute the majority of clones derived from cells sensitized to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines. The implications of the derivation and function of HITc clones are discussed.

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