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Epstein–Barr virus (EBV), a member of the family Herpesviridae, is widely spread in the human population and has the ability to establish lifelong latent infection. In immunocompetent individuals the virus reactivation is usually harmless and unnoticeable. In immunocompromised patients productive infection or type III latency may lead to EBV-associated post-transplant lymphoproliferative disorder (PTLD). The aim of our research was to investigate the utility of PCR-based methods in the diagnosis and monitoring of EBV infections in bone marrow transplant recipients. Thirty-eight peripheral blood leukocyte samples obtained from 16 patients were analysed, in which EBV DNA was confirmed by PCR. We used semi-quantitative PCR to estimate the viral load and reverse-transcription PCR (RT-PCR) to differentiate between latent and productive EBV infection. In 14 patients we confirmed productive viral infection. We observed a correlation between higher number of EBV genome copies and the presence of transcripts specific for type III latency as well as clinical symptoms.
The aim of this study was to compare the prevalence of EBV genotype and del-LMP-1 in saliva from Polish, Taiwanese and Arabic healthy students. The study group consisted of 56 healthy students; 24 of them Polish, 25 Taiwanese, and 7 Arabic. Typing was carried out using PCR with EBNA-2 primers. A detection of LMP-1 variants was also performed using PCR. EBV DNA was detected in 22 investigated samples (39.3%). Type 1 of the virus was dominant in both Polish and Taiwanese group. Among 62.5% Tai wanese with EBV 1 and 55.6% Polish detected EBV with 30-bp deletion in LMP-1 gene.
Epstein-Barr virus (EBV) is a ubiquitous virus with infections commonly resulting in a latency carrier state. Although the exact role of EBV in cancer pathogenesis remains not entirely clear, it is highly probable that it causes several lymphoid and epithelial malignancies, such as Hodgkin’s lymphoma, NK-T cell lymphoma, Burkitt’s lymphoma, and nasopharyngeal carcinoma. EBV-associated malignancies are associated with a latent form of infection, and several of these EBV-encoded latent proteins are known to mediate cellular transformation. These include six nuclear antigens and three latent membrane proteins. Studies have shown that EBV displays distinct patterns of viral latent gene expression in these lymphoid and epithelial tumors. The constant expression of latent membrane protein 2A (LMP2A) at the RNA level in both primary and metastatic tumors suggests that this protein might be a driving factor in the tumorigenesis of EBV-associated malignancies. LMP2A may cooperate with the aberrant host genome, and thereby contribute to malignant transformation by intervening in signaling pathways at multiple points, especially in the cell cycle and apoptotic pathway. This review summarizes the role of EBV-encoded LMP2A in EBV-associated viral latency and cancers. We will focus our discussions on the molecular interactions of each of the conserved motifs in LMP2A, and their involvement in various signaling pathways, namely the B-cell receptor blockade mechanism, the ubiquitin-mediated (Notch and Wnt) pathways, and the MAPK, PI3-K/Akt, NK-κB and STAT pathways, which can provide us with important insights into the roles of LMP2A in the EBV-associated latency state and various malignancies.
Epstein-Barr virus (EBV) establishes latency in the resting memory B-cell compartment. It has been recently suggested that maintenance of chronic infection is dependent on periodic reactivation. Although the stimuli for EBV reactivation in vivo during natural infections are largely unknown, there is evidence indicating that heterologous infections could trigger herpesviruses reactivation. The purpose of this work was to identify the influence of Toll-like receptors stimulation on EBV replication in EBV latently infected Burkitt lymphoma cells (P3HR-1, Raji and Namalwa). The cells were stimulated with Pam3CSK4 (synthetic triacylated lipoprotein), PolyI:C (synthetic analog of dsRNA), LPS (lipopolysaccharide from E.coli), measles virus (MeV) and PMA (phorbol myristate acetate). Non-stimulated cells (NS) served as control. EBV expression was investigated at mRNA level for three viral lytic genes: BZLF1 (immediate early, ZEBRA), BALF2 (early, EA) and BcLF1 (late, VCA). Additionally, the effect of stimulation on NF-kBp65 and inflammatory cytokines (IL-1b, IL-6, IL-8, IL-10, IL-12p70, and TNF) was investigated. Stimulation of TLRs led to limited changes in EBV expression manifesting as increase of ZEBRA at mRNA level in cells treated with PolyI:C and Pam3CSK4. Stimulation with PolyI:C, Pam3CSK4 and LPS also lead to considerable increase of NF-kBp65, while increased levels of inflammatory cytokines were observed for IL-8, TNF and IL-6 in cells treated with PMA and MeV. In conclusion, the results of our experiments support the suggestion that TLRs stimulation with microbial ligands influences EBV virus replication.
In 48 adult women, subdivided into group 1 with no cervical intraepithelial neoplasia (CIN-negative) and group 2 (CIN-positive), endocervical scrapes were tested for the presence EBV DNA and HPV DNA using PCR-ELISA. In addition, attempts were made to detect HPV 16 and HPV 18 using other PCR amplification techniques. In parallel, in biopsies of uterine cervix obtained from group 2 patients, presence of EBER was documented by RNA in situ hybridization (ISH). Sera of all patients were tested for anti-EBV antibodies. In group 1, presence of EBV DNA was noted in the material obtained from 8 women (30.8%), while HPV DNA was detected in 2 women (7.7%). In group 2, EBV DNA was present in the material obtained from 11 patients (50%), including 7 (31.8%) with HPV DNA also identified. In 5 women (22.7%) of group 2 only HPV DNA was detected. The identifical HPV DNA in all cases belonged to HPV 16 type. Both in group 1 and in group 2, all patients were found to carry serum IgG-anti-VCA and IgG-anti-EBNA antibodies. The results allow to conclude that, co-infection with EBV and HPV 16 may be of cervical significance in etiopathogenesis of uterine cervical cancer.
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