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Table 1 summarizes the timing of first appearance, dominance, completeness, and loss of mutations among two types of Gag mutations, reverse mutations and escape mutations from the wild type.
The medians (IRQ) of completeness were 152 (100–176) days p/s and 243 (101–370) days p/s for reverse mutations and escape mutations from the wild type, respectively (p = 0.001).
Taking into account the correlation among an individual subject's values, we fit a Cox proportional hazards models with frailties to compare time to first appearance (dominance, or completeness) for reverse mutations and escape mutations from the wild type.
The time of appearance of the total reverse mutations and escape mutations from the wild type did not significantly differ within subset of the de novo mutations (p = 0.16), but was shorter for pre-existing reverse (p = 0.044) mutations in Gag.
The time of appearance of minor mutations was 312 (160–418) days p/s and 349 (240–415) days p/s for reverse and escape mutations, respectively (p = 0.031), while appearance of transient mutations did not differ significantly between reverse mutations and escape mutations from the wild type.
There are several mechanisms whereby cancer cells can obtain uncontrolled ErbB receptor signaling, including increased receptor expression, activating mutations, and escape of endocytic receptor downregulation (Bache et al. 2004; Citri and Yarden 2006; Normanno et al. 2005; Polo et al. 2004; Warren and Landgraf 2006).
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The results of our studies seem to resolve the discrepancy in understanding of relationships between HIV-1 reverse mutations to and escape mutations from the wild type sequence highlighted recently by Brumme & Walker [54].
There's the problem of mutation and escape from protection from one vaccine, a whole series of things that will maintain infectious diseases as a problem, but hopefully in developing countries not the problem that it is today where over a third of the population dies from infectious disease.
Due to the low density of envelope spikes with restricted mobility present on the surface of HIV virus, which limit the antibody potency and allow virus mutation and escape from the immune system, it is important for a neutralizing antibody to form bivalent or multivalent bonds with the virus.
Consequently, new variants must arise by mutation and escape the repression mechanism before degenerating.
HIV mutation and escape from CD8 T-cell responses, when detected, have been associated with subsequent disease progression [ 9– 11].
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Justyna Jupowicz-Kozak
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