PMID- 1846816
OWN - NLM
STAT- MEDLINE
DCOM- 19910314
LR  - 20141120
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 21
IP  - 1
DP  - 1991 Jan
TI  - Inhibition of tumor necrosis factor-alpha transcription by Epstein-Barr virus.
PG  - 203-8
AB  - Tumor necrosis factor-alpha (TNF-alpha), which is produced mainly by 
      monocyte/macrophage cells, has diverse physiological functions on lymphoid cells. 
      Moreover, it has been shown that TNF-alpha exhibits antiviral activities. Here we 
      report that Epstein-Barr virus (EBV), a B lymphotropic human herpes virus that 
      interacts intimately with the immune system, exerts a strong inhibitory effect on 
      TNF-alpha production by lipopolysaccharide-treated peripheral blood leukocytes as 
      well as by monocytic cell lines, HL-60 and U-937. Flow cytometric analysis 
      following staining with OKB7 monoclonal antibody showed that about 20% of cells 
      from these monocytic lines express the CR2 antigen. Direct binding of fluorescein 
      isothiocyanate-labeled EBV indicated that the virus binds to approximately 22% of 
      cells of both monocytic lines. However, no virus-specific antigens were detected 
      in the infected cells by immunofluorescence, suggesting that the infection was of 
      the abortive type. The use of UV- or heat-inactivated EBV and inhibitory effect 
      on TNF-alpha synthesis. These results suggest that infectious virus is necessary 
      to obtain such an inhibitory effect. Analysis of TNF-alpha mRNA by polymerase 
      chain reaction amplification indicated that the EBV suppressive effect is 
      manifested at the transcriptional level. In contrast, EBV did not inhibit 
      interleukin 1 mRNA production by these cells. These results indicate that EBV 
      interacts directly with monocytes/macrophages to exert its immunomodulatory 
      effect.
FAU - Gosselin, J
AU  - Gosselin J
AD  - Department of Microbiology and Immunology, University of Montreal, Quebec, 
      Canada.
FAU - Menezes, J
AU  - Menezes J
FAU - D'Addario, M
AU  - D'Addario M
FAU - Hiscott, J
AU  - Hiscott J
FAU - Flamand, L
AU  - Flamand L
FAU - Lamoureux, G
AU  - Lamoureux G
FAU - Oth, D
AU  - Oth D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, Differentiation, B-Lymphocyte)
RN  - 0 (Interleukin-1)
RN  - 0 (Oligonucleotides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Complement)
RN  - 0 (Receptors, Complement 3d)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antibodies, Monoclonal/immunology
MH  - Antigens, Differentiation, B-Lymphocyte/metabolism
MH  - Base Sequence
MH  - *Gene Expression Regulation, Viral
MH  - Herpesvirus 4, Human/*genetics
MH  - Humans
MH  - In Vitro Techniques
MH  - Interleukin-1/biosynthesis
MH  - Molecular Sequence Data
MH  - Oligonucleotides/chemistry
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/genetics
MH  - Receptors, Complement/metabolism
MH  - Receptors, Complement 3d
MH  - Transcription, Genetic
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*genetics
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - 10.1002/eji.1830210130 [doi]
PST - ppublish
SO  - Eur J Immunol. 1991 Jan;21(1):203-8. doi: 10.1002/eji.1830210130.