Sentence examples for model of latency from inspiring English sources

In a recent study, University of Michigan doctoral student Elaine Wah and I developed a simple model of latency arbitrage across two exchanges with a delayed public ticker.

The reactivation for the complexes is shown here for the U1 promonocytic cell line model of latency as proof of concept that the cytostatic compounds also reactivate virus like HU.

In the latently infected cell lines, ACH2 and U1, belinostat has activity against class I and II HDACs with similar potency to givinostat, and also displayed ability to induce HIV production at therapeutic concentrations in a primary CD4+ T cell model of latency (Rasmussen et al., unpublished).

Further studies are needed to validate the hypoxic models of latency and identify mechanisms used by MTB to enter into, persist in, and exit from latent disease states.

Several primary CD4+ T-cell models of latency exist where activated cells are infected and subsequently allowed to return to a quiescent latently infected state.

In primary T cell models of latency, specific IS are associated with intracellular viral antigen expression that is not directly related to cell activation.

A correlation between viral antigen expression and specific genomic markers has been shown within different in vitro models of HIV latency, but the correlations have not translated to the general features of IS that extend across multiple models of latency in primary CD4+ T cells.

The in vitro models of latency have characterized factors affecting proviral expression including orientation of the provirus [ 19] with neighboring host genes as well as TI [ 47] and epigenetic modifiers.

In this review, we focus on understanding the effect of HIV-1 integration in the in vitro models of latency and the recent data identifying some IS that may directly determine the persistence of latency either by favoring infected cell survival or by maintaining low viral expression.

In the most extensive study of integration sites in silent and productive sites in primary T cells in five different models of latency [ 66], the epigenetic modifiers at the site of HIV integration even when in an actively transcribed gene had only a modest effect in determining the level of expression, and no consistent features could be demonstrated across the different models.

Study of the cellular and molecular establishment of the latent reservoir has used in vitro models of latency in cell lines and primary CD4+ T cells and analysis of residual HIV in resting CD4+ T cells from HIV-infected patients on cART.