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1 IL-10 is associated with decreased gammaHV68 long-term latency.
2 is possible to effectively vaccinate against long-term latency.
3 in germinal center and memory B cells during long-term latency.
4 after infection but was undetectable during long-term latency.
5 does not prevent gammaHV68 from establishing long-term latency.
6 ng early latency and immature B cells during long-term latency.
7 cess to memory B cells, a major reservoir of long-term latency.
8 ed in a variety of cell populations but that long-term latency (6 months postinfection) in the spleen
10 activation of ERK-MAPK signaling impacts on long-term latency and reactivation in hematopoietic cell
11 response against gammaherpesviruses to alter long-term latency and suggest that limiting long-term la
12 ual evoked potential (mfVEP) technique after long-term latency changes in optic neuritis (ON)/multipl
13 , our work shows how tumor recurrences after long-term latency evolve toward T-cell resistance by ind
14 tion and short-term latency but cannot alter long-term latency further call into question the possibi
15 s during the acute infection and establishes long-term latency in B cells and lung epithelial cells.
17 o PCs after infection by EBV, thus favouring long-term latency in MBC and asymptomatic persistence.
18 is established in a variety of cell subsets, long-term latency in the lung is only maintained in B ce
22 ablished in germinal center B cells and that long-term latency is preferentially maintained in two di
24 wnregulation of viral gene expression in the long-term latency reservoir is likely to facilitate evas
25 ce proteins is turned off in the predominant long-term latency reservoir of resting memory B cells, s
26 BV infection, including the establishment of long-term latency within B lymphocytes, and is therefore
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