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1 ssed in a minimal number of cells to promote virus latency.
2 silence the activity of this promoter during virus latency.
3 molecularly indistinguishable from wild-type virus latency.
4 that was molecularly identical to wild-type virus latency.
5 resident progenitors are important sites of virus latency.
6 alogous to the several types of Epstein-Barr virus latency.
7 ly at peripheral nerves, the natural site of virus latency.
8 t also display one of two different forms of virus latency.
9 ) can promote transcriptional repression and virus latency.
10 It is protective by ensuring maintenance of virus latency after infection, yet deleterious by recrui
11 sion may shed light on the mystery of animal virus latency and that strategies to manipulate noise ma
12 has revealed a complex relationship between virus latency and the stage of B cell differentiation.
13 may be a novel target for the disruption of virus latency and therefore the treatment of gammaherpes
14 nd the associated signal molecules in herpes virus latency and uncover a novel paradigm that shows th
17 nds of alpha v beta6 (foot-and-mouth-disease virus, latency associated peptide), have a common struct
18 h the Notch interacting protein Epstein-Barr virus latency C promoter binding factor-1, suppressor of
19 n (NICD), which associates with Epstein-Barr virus latency C-promoter binding factor-1/suppressor of
23 w here for the first time that during LAT(+) virus latency, most of the HSV-1-specific TG resident CD
26 express viral EBNA-1 and other Epstein-Barr virus latency-related elements for their survival, their
27 may be more important for the maintenance of virus latency than the less abundantly transcribed and r
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