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There are exposures of target cells to virus that fail to initiate an infection, and there is spread of virus from the initially infected cell(s) that fails to become a systemic infection, collectively adding a bias to the distribution of polymorphisms in the transmitted/founder virus population.
Genital herpes can facilitate HIV-1 acquisition by disrupting the epithelial barrier, thereby increasing exposure of target cells to virus [2], [17] [18].
As indicated, in some experiments 5% PEG was added during 16 h exposure of cells to virus (and inhibitor), a strategy that increased the number of infected cells by at least 15-fold [30].
Therefore, we conclude that the sensitivity of Lec1 cells to virus infection and fusion appears to be a feature of NDV.
The number has been estimated from HA titers from various experiments of our group (data not shown) with influenza virus (NIBSC) assuming that for the respective HA value the ratio of red blood cells to virus particles is 1 1.
These results suggested the improved assay was able to eliminate both the effect of the unknown factors in plasma (or sera) on anti-HIV-1 neutralization and prolong time exposure cells to virus and plasma (or sera).
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These results suggest that ABT-263 and its structural analogues sensitise cells to virus-mediated killing and confirmed that Bcl-xL, Bcl-2 and Bcl-w are essential for cell survival upon viral infection.
Susceptibility of different cells to viruses depends on several factors.
I thus encourage the authors to consider the two alternative possibilities in the discussion of their results, either LGT from cells to viruses or from viruses to cells.
As a consequence, the authors systematically favour in this paper transfers from cells to viruses to explain the origin of NCLDV ligases.
However, we realize that HGT from cells to viruses harboring smaller proteomes or RNA genomes might be occurring at different (or higher) levels.
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