NucliSENS EasyQ HPV v1 test - Testing for oncogenic activity of human papillomaviruses.

Background: Analytical sensitivity of DNA-based assays to detect infection with human papillomaviruses is very high, but clinical specificity for cervical cancer strongly depends on the age of the patient and case classification. To solve the dilemma between sensitivity and specificity, a new generation of assays focuses on the pathogenic factors that underlie the development of HPV-associated tumors: the expression of the viral oncogenes E6 and E7. Demonstration of persistent expression of these mRNAs or expression in the context of relevant clinical symptoms has a strong positive predictive value for the development of HPV-associated carcinomas and strongly warrants further diagnostic action.

High-resolution analysis of CpG methylation and in vivo protein-DNA interactions at the alternative Epstein-Barr virus latency promoters Qp and Cp in the nasopharyngeal carcinoma cell line C666-1.

Transcripts for the Epstein-Barr virus (EBV) encoded nuclear antigens (EBNAs) are initiated at alternative promoters (Wp, Cp, for EBNA 1-6 transcripts and Qp, for EBNA 1 transcripts only) located in the BamHI W, C or Q fragment of the viral genome. To understand the host-cell dependent expression of EBNAs in EBV-associated tumors (lymphomas and carcinomas) and in vitro transformed cell lines, it is necessary to analyse the regulatory mechanisms governing the activity of the alternative promoters of EBNA transcripts. Such studies focused mainly on lymphoid cell lines carrying latent EBV genomes, due to the lack of EBV-associated carcinoma cell lines maintaining latent EBV genomes during cultivation in tissue culture.

A 30 kb region of the Epstein-Barr virus genome is colinear with the rearranged human immunoglobulin gene loci: implications for a "ping-pong evolution" model for persisting viruses and their hosts. A review.

The left part of the Epstein-Barr virus (EBV) genome exhibits a strong colinearity of structural and functional elements with the immunoglobulin (Ig) gene loci which is only partially reflected in nucleotide sequence homologies. We propose that this colinearity may be the result of an inter-dependent co-evolution of the immunoglobulin loci together with EBV. Our observation could help elucidating the mechanisms of somatic hypermutation, explaining the ability of EBV to accidentally cause tumors, and shedding more light on the general mechanisms of viral and organismal evolution.

Monoclonal gammopathy of undetermined significance (MGUS) is associated with an increased frequency of Epstein-Barr Virus (EBV) latently infected B lymphocytes in long-term renal transplant patients.

Monoclonal gammopathy of undetermined significance (MGUS) is a common phenomenon in kidney transplant patients that might be a prestage of posttransplant lymphoproliferative disease (PTLD). Because the role of Epstein-Barr virus (EBV) for PTLD development is well established, we wondered about the association between EBV and MGUS. Thus, B-cells from kidney transplant patients (25 with and 100 without MGUS) and from 100 healthy controls were analyzed for EBV latent (EBER1) and lytic (EA, VCA) gene expression by RT-nested PCR.

The LCR of EBV makes Burkitt's lymphoma endemic.

The spectacular ability of Epstein-Barr virus (EBV) to immortalize and morphologically transform human B cells in vitro to lymphoblastoid cell lines (LCLs) is central to most molecular models of viral oncogenesis. However, binding of transcription factor and oncoprotein c-Myc to the major locus control region (LCR) of the viral genome directs us to an alternative model for the origin of Burkitt's lymphoma (BL). In this model, improved nuclear maintenance of the viral genome and the continuous expression of anti-apoptotic functions in B cells exhibiting class I EBV latency contribute to the generation of BL, without any detour through EBV nuclear antigen (EBNA) 2-driven B-cell immortalization (also called class III latency).