Sentence examples for models of latency from inspiring English sources

Overall, our results demonstrate that latent HIV infection and the subsequent reactivation of viral proteins increase phospho-signaling following T cell activation, as observed across two experimental models of latency.

While some studies demonstrated modest differences in gene expression41 and kinase activity5, these studies used long-established cell line models of latency, making it difficult to assess whether these differences arose due to cell line divergence.

Thus, PLS-DA showed that the phosphorylation signatures following T cell activation were sufficient to distinguish infected and uninfected cells across both primary cultured TCM cells and Jurkat T cell line models of latency.

We provide evidence that latent and reactivating HIV infection is associated with changes in signal transduction in both primary cultured CD4+ TCM cells and Jurkat cell line models of latency (Figs. 1 2), even though basal phosphorylation levels of the five pathways measured are indistinguishable (Supplementary Fig. S2).

We compared phospho-signaling between uninfected and latently infected cells in both primary cultured TCM and Jurkat cell models of latency, because we assumed that trends conserved across experimental latency models are more likely to represent the in vivo latent memory T cell reservoir.

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.

To complement this model, we used a Jurkat model of latency that responds to TCR stimulation, because such models have LRA responses that are more similar to patient T cells treated ex vivo than most other primary T cell models27.

Due to the high degree of variability that experimental HIV latency models exhibit in response to LRA stimulation27, we compared our results to a Jurkat T cell line model of latency and its uninfected parental Jurkat cell line to identify conserved changes.

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).