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Although ETVr could presumably also involve enhanced replication through adaptive changes, the fact that resistance was observed through reduced ETV utilization and that resistant HBV and polymerase did not have enhanced replicative capacity, argue against the adaptive mechanism for resistance.
Strikingly, the G28A mutant virus also replicated in Huh-7.5 cells expressing the miR-122 decoy (Fig. 3a), demonstrating that a single mutation in the HCV genome enhanced replication in the setting of miR-122 decoy expression.
Recombinant viruses encoding various combinations of these Vero cell adaptation mutations did not demonstrate enhanced replication in Vero cells over that exhibited by the single mutations.
A single NS5B M31I substitution enhanced replication to levels sufficiently robust to quantify sensitivity to HCV inhibitors in a transient replication assay.
To exclude that the observed resistance is the result of generally enhanced replication, the replication fitness of each mutant was compared to that of WT replicon.
Both use enhanced replication mechanisms to warrant the integrity of data including the prevention of loss.
Similar(45)
PARI depletion enhances replication stress and DNA-damage accumulation, coupled with increased myeloid differentiation.
These results indicate that A92K reduced virus replication but that R30Q compensated for it mainly by enhancing infectious virus production and partially by enhancing replication.
Phosphorylation of viral proteins plays important roles in enhancing replication and inhibition of normal host-cell functions.
Continued passage led to mutations in the non-structural genes although these mutations did not significantly enhance replication of the original replicon.
All cell lines contained novel substitutions within NS5B which were subsequently engineered into the parental 1b:2b replicon and shown to enhance replication to various degrees.
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