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At MOI of 1, 30% of human T cells supported virus entry, which was completely blocked by the CCR5 inhibitor TAK-779.
Our data suggest that pigs and chickens of the age used in the experiment were infected with SARS-CoV and, to a very limited degree, supported virus replication.
HepG2 cells expressing T149A, E152A or T153A CD81 mutants showed minimal evidence for HCVpp infection, whereas cells expressing K148A or K148A/T149A CD81 supported virus infection at comparable levels to WT CD81 (Fig. 4D).
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However, Nemo −/− MEF cells stably expressing NEMO 6KR (K111/285/309/325/342/344R) mutant still supported virus-induced cytokine production similar to those expressing wild-type NEMO.
Here we report that continuous treatment with PEG following initial infection of HepG2-NTCP cells increases the efficiency of infection by supporting virus spread to uninfected cells.
The retroviral life cycle requires that viral proteins co-opt host factors to support virus production.
It is therefore crucial that normal liver cells do not support virus replication.
However, rat T cells were unable to support virus spreading due to putative post-transcriptional blocks [5].
Under these conditions, mouse T cells are therefore far less efficient than human T cells in supporting virus integration.
Nevertheless, virus replication in neighbouring cells was consistently observed at the majority of bombardment sites following complementation with eIF4ES and was used as a measure of the effectiveness of mutant eIF4E derivatives to support virus multiplication (replication and movement).
In addition, 29 of the 41 significantly regulated genes with putative metabolic functions were up-regulated, perhaps indicating a shift in the metabolic state of the cell to support virus replication [19].
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