Epstein-Barr virus induces an oxidative stress during the early stages of infection in B lymphocytes, epithelial, and lymphoblastoid cell lines

被引:74
作者
Lassoued, Saloua [1 ]
Ben Ameur, Randa [1 ]
Ayadi, Wajdi [2 ]
Gargouri, Bochra [1 ]
Ben Mansour, Riadh [1 ]
Attia, Hammadi [1 ]
机构
[1] Inst Super Biotechnol Sfax, Unite Biotechnol & Pathol, Sfax 3038, Tunisia
[2] Hop Habib Bourguiba, Microbiol Lab, Fac Med, Sfax, Tunisia
关键词
catalase; superoxide dismutase; oxidative stress; Epstein-Barr virus infection; B cells; epithelial cells; MDA;
D O I
10.1007/s11010-008-9755-z
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The study investigates the direct effect of Epstein-Barr virus infection on the oxidative profile of in vitro cultivated human cells. For this purpose, a panel of human EBV target cells presenting heterogeneity in their cellular and culture types (epithelial cells or lymphocytes; primary culture or continuous cell culture) was selected. These cells are purified human B lymphocytes, DG75, 293, and HepG2 cell lines. The oxidative stress was evaluated during the early stages of infection (2, 12, and 24 h) by measuring malondialdehyde, the end product of the lipid peroxidation, as well as the activities of two antioxidant enzymes: catalase and superoxide dismutase. The obtained results were compared with those of the untreated cells and the K562 cell line which has no interaction with EBV. The incubation of the different target cells with EBV induced an oxidative stress in the purified B lymphocytes, DG75, and 293, but not in HepG2 and K562. This oxidative stress was highlighted by an increase in MDA level (P < 0.05), which began 2 h after the addition of the virus and persisted after 12 and 24 h. Simultaneously, a decrease in catalase and superoxide dismutase activities was observed (P < 0.05), suggesting an alteration of the molecular mechanisms promoting cellular resistance to reactive oxygen species (ROS). The efficiency of EBV infection, assessed by viral DNA PCR amplification, was confirmed in 293 and DG75 but not in HepG2, which was in total concordance with their oxidative profiles. In conclusion, the EBV infection of B and epithelial cells leads to the establishment of an oxidative stress which can play a key role during the viral transformation.
引用
收藏
页码:179 / 186
页数:8
相关论文
共 47 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]  
Behrend L, 2003, BIOCHEM SOC T, V31, P1441
[3]   ESTABLISHMENT IN CONTINUOUS CULTURE OF A NEW TYPE OF LYMPHOCYTE FROM A BURKITT-LIKE MALIGNANT-LYMPHOMA (LINE DG-75) [J].
BENBASSAT, H ;
GOLDBLUM, N ;
MITRANI, S ;
GOLDBLUM, T ;
YOFFEY, JM ;
COHEN, MM ;
BENTWICH, Z ;
RAMOT, B ;
KLEIN, E ;
KLEIN, G .
INTERNATIONAL JOURNAL OF CANCER, 1977, 19 (01) :27-33
[4]   Increased oxidative stress associated with the severity of the liver disease in various forms of hepatitis B virus infection [J].
Bolukbas, C ;
Bolukbas, FF ;
Horoz, M ;
Aslan, M ;
Celik, H ;
Erel, O .
BMC INFECTIOUS DISEASES, 2005, 5 (1)
[5]   Oxidative stress triggers STAT3 tyrosine phosphorylation and nuclear translocation in human lymphocytes [J].
Carballo, M ;
Conde, M ;
El Bekay, R ;
Martín-Nieto, J ;
Camacho, MJ ;
Monteseirín, J ;
Conde, J ;
Bedoya, FJ ;
Sobrino, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (25) :17580-17586
[6]   Reactive oxygen signaling and MAPK activation distinguish Epstein-Barr virus (EBV)-positive versus EBV-negative Burkitt's lymphoma [J].
Cerimele, F ;
Battle, T ;
Lynch, R ;
Frank, DA ;
Murad, E ;
Cohen, C ;
Macaron, N ;
Sixbey, J ;
Smith, K ;
Watnick, RS ;
Eliopoulos, A ;
Shehata, B ;
Arbiser, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (01) :175-179
[7]   Oxidative injury to endothelial cells due to Epstein-Barr virus-induced autoantibodies against manganese superoxide dismutase [J].
Dalpke, AH ;
Thomssen, R ;
Ritter, K .
JOURNAL OF MEDICAL VIROLOGY, 2003, 71 (03) :408-416
[8]   EPSTEIN-BARR VIRUS-RNA IN BURKITT TUMOR TISSUE [J].
DAMBAUGH, T ;
NKRUMAH, FK ;
BIGGAR, RJ ;
KIEFF, E .
CELL, 1979, 16 (02) :313-322
[9]  
FINGEROTH JD, 1973, J VIROL, V293, P2115
[10]  
GORDON J, 1986, IMMUNOLOGY, V58, P591