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1 CD4 T cell immunity in controlling varicella virus latency.
2 ssed in a minimal number of cells to promote virus latency.
3 silence the activity of this promoter during virus latency.
4 molecularly indistinguishable from wild-type virus latency.
5  that was molecularly identical to wild-type 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  resident progenitors are important sites of virus latency.
9 t also display one of two different forms of virus latency.
10 ) can promote transcriptional repression and virus latency.
11  It is protective by ensuring maintenance of virus latency after infection, yet deleterious by recrui
12       This work indicates that regulation of virus latency and reactivation is cell type specific.
13 sion may shed light on the mystery of animal virus latency and that strategies to manipulate noise ma
14  has revealed a complex relationship between virus latency and the stage of B cell differentiation.
15  may be a novel target for the disruption of virus latency and therefore the treatment of gammaherpes
16 nd the associated signal molecules in herpes virus latency and uncover a novel paradigm that shows th
17 athways that are critical for cell survival, virus latency, and growth transformation.
18         Because features of varicella-zoster virus latency are similar in primate and human ganglia,
19 nds of alpha v beta6 (foot-and-mouth-disease virus, latency associated peptide), have a common struct
20 h the Notch interacting protein Epstein-Barr virus latency C promoter binding factor-1, suppressor of
21 n (NICD), which associates with Epstein-Barr virus latency C-promoter binding factor-1/suppressor of
22 CD4 T cell immunity in controlling varicella virus latency.IMPORTANCE Reactivation of latent VZV in h
23 n results in a complete failure to establish virus latency in the spleens of laboratory mice.
24 n the respiratory tract, but asymptomatic BK virus latency is established in the urothelium.
25                   Disruption of Epstein-Barr virus latency is induced by expression of either the BZL
26 ar infection dynamics, suggesting that giant virus latency is prevalent in natural host communities.
27       However, using different doses of each virus, latency levels, time of reactivation, and T cell
28 w here for the first time that during LAT(+) virus latency, most of the HSV-1-specific TG resident CD
29 tivity is explained by a unique LEC-specific virus latency program.
30  (TBP) were identified on the herpes simplex virus latency promoter in previous work.
31  express viral EBNA-1 and other Epstein-Barr virus latency-related elements for their survival, their
32 may be more important for the maintenance of virus latency than the less abundantly transcribed and r
33                    The restriction of herpes virus latency to mammalian sensory ganglia has led to a