Rebecca Skalsky (Oregon Health and Science University, USA)“Regulation of Host Signaling Pathways by EBV miRNAs” EBV encodes 25 precursor miRNAs ~100-200 different target sites on mRNAs> 44 EBV miRNAs =significan tregulatory potential MiRNAs are great toools for viruses:– non-immunogenicity– -require limited encoding capacity (only 22 not)-can rapidly evolve; have Lymphocryptoivirus muRNAs are highly conserves Circular […]

Bill Sugden (McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, USA) “How EBV Prevails During Productive Infection” Hybrid of P3HR1 and D98. (Endogenous P3HR1 cells) EBV’s lyticv phase commandeers the cell much as do a-herpesviruses Determining when vEBV DNA amplifies following induction off the productive cycle (treated cells with tamoxifen —> BZLF 1 expression) Tamoxifen was

Paul Farrell (Imperial College London, United Kingdom) –”EBV Genome Sequence Variation: Geography, Function and Disease” J Virol. 2017 Jul 12;91(15). Natural Variation of Epstein-Barr Virus Genes, Proteins, and Primary MicroRNA.   (PubMed Link) 138 new EBV genomes, 125 of these combined with 116 others = 241 Analysis of 241 aligned EBV genomes in multiple sequence alignment Type1/Type2

Irving Weissman (Stanford University School of Medicine, USA) “Normal and Neoplastic Stem Cells” Marrow or MPB (mobilized peripheral blood) Mixture of cells: HSCs, T cells, cancer cells Deplete mature blood cells by labeling with magnetic antibodies Pure HSCs for transplantation 250,000 fold depletion an ever cells or T cells Unwanted cells : cancer cells, T

Patrick Moore (University of Pittsburgh, USA)  “Why Do Viruses Cause Cancer?” PubMed Link (pdf 2803) Viruses do not “mean” to cause cancer • Cancer endangers virus as well as host • Viruses non-transmissible in tumors (eg latency, pseudo-latency) • Virus populations Limited resource hypothesis: enhancing lyric virus replication tumor virus targets at G1 phase Infection is