Abstract
Viral infections have been implicated in the pathogenesis of multiple sclerosis. Epstein-Barr virus (EBV) has frequently been investigated as a possible candidate and torque teno virus (TTV) has also been discussed in this context. Nevertheless, mechanistic aspects remain unresolved. We report viral replication, as measured by genome amplification, as well as quantitative PCR of two TTV-HD14 isolates isolated from multiple sclerosis brain in a series of EBV-positive and -negative lymphoblastoid and Burkitt's lymphoma cell lines. Our results demonstrate the replication of both transfected TTV genomes up to day 21 post transfection in all the evaluated cell lines. Quantitative amplification indicates statistically significant enhanced TTV replication in the EBV-positive cell lines, including the EBV-converted BJAB line, in comparison to the EBV-negative Burkitt's lymphoma cell line BJAB. This suggests a helper effect of EBV infections in the replication of TTV. The present study provides information on a possible interaction of EBV and TTV in the etiology and progression of multiple sclerosis.
Highlights
The pathogenesis of multiple sclerosis (MS) is probably triggered by a combination of genetic and environmental factors [1,2,3,4,5]
We have transfected the full-length genomes of two TT viruses isolated from brain tissue from an MS patient in order to ascertain first, whether viral replication takes place in different B lymphocytic and Burkitt’s lymphoma cell lines and, secondly, to determine whether Epstein-Barr virus (EBV) acts as a helper virus for the replication of torque teno virus (TTV)
We observed that the replication pattern of both TT viruses is cell-type dependent with higher levels of replication measured in the EBV positive cell lines, but showing variability in the DDCt at certain time points (Figure 2)
Summary
The pathogenesis of multiple sclerosis (MS) is probably triggered by a combination of genetic and environmental factors [1,2,3,4,5]. Children experiencing viral infections later in life are at risk for developing this disease [1,3,4,7,8,9]. An upregulation of the endogenous retroviruses HERV-H and HERV-W transcription was mediated by herpesviruses Herpes simplex-1 (HSV1), human herpesvirus-6 (HHV-6) and VZV [22,23]. A more direct role for HHV-6 in MS was suspected [24,25], but was subsequently questioned because no difference was observed in the HHV-6 prevalence between cases and controls [26,27], its possible role prior to onset of disease was not excluded [28]. Mechanistic aspects through which EBV infections may participate in the pathogenesis of MS remain elusive, despite the compelling epidemiological data available [32,33]
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