Journal of Virology · 1992 · 249 citations · 32 references
Life SciencesImmunologyInfectious DiseasesGene ExpressionImmunogeneticsVirologyB Cell BiologyCell-type Specific Gene ExpressionViral Gene ExpressionEpstein-barr Virus LatencyEpstein-barr Virus PersistenceLatency In B CellsPromoter-associated RnasViral Gene Expression In LatencyViral Mrna Splicing
In this study of Epstein-Barr virus (EBV) latency, the polymerase chain reaction was used in modified form for amplification and detection of viral mRNA sequences in peripheral blood lymphocytes from healthy seropositive adults. Six known promoters for latent gene expression and eight known gene products were identified in in vitro-immortalized lymphocytes and in the cell lines established spontaneously from seropositive adults. We examined whether mRNA expression in uncultured B cells from four seropositive adults was the same as that which occurred in spontaneously established EBV-positive B-cell lines from the same individuals. A minimum of 17 polymerase chain reaction targets was required to circumscribe the known latent mRNA structures. Expression of the C promoter for the EBNA genes was detected in B-cell RNA from three of the four subjects. Transcripts initiated from the alternative W promoter for EBNA expression were not detected. The spliced transcripts detected in the B cells contained only the C2-to-W1 alternative splice, which was nonproductive for EBNA4 gene expression. None of the other EBNA open reading frames were detected spliced onto the 3' ends of the C promoter-initiated RNAs. Spliced RNA from the TP gene was detected in all four subjects. Expression of the TP gene was restricted to TP1 promoter-initiated RNAs, as no TP2 promoter-initiated transcripts were detected. Expression of RNA from the LMP gene was not detected. The F promoter which is active in the restricted expression latency that occurs in Burkitt's lymphoma cells was not detected being expressed in peripheral blood B cells. This pattern of latent gene expression is unique to uncultured B cells, indicating that there are profound differences between viral latent states in vitro and in situ and suggesting a central role for the TP gene in the latency of EBV.
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Christopher D. Gregory, R J Murray, C. Edwards et al. · The Journal of Experimental Medicine · 1988 · 339 citations · Full text
Life Sciences, Immunology, Oncology +17
Denis J. Moss, Alan B. Rickinson, J. H. Pope · International Journal of Cancer · 1978 · 297 citations