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Only a few sites showed significantly lower viral loads for individuals who presented rare residues at interacting conserved sites (Table 1), nonetheless, the trend toward lower viral loads may suggest that the presence of rare residues resulted in viruses with poorer replication capacities.
The contrasting clinical phenotypes of nonprogressive vs progressive disease course associated with carriage of a HLA-B*57 allele has been attributed to differences in cytotoxic T lymphocyte (CTL) escape mutations and CTL activity against epitopes in Gag as well as to differential viral replication capacities [20], [22].
In contrast, the tested recombinants and parental BoHV-1.2ΔgCΔgI displayed reduced in vivo replication capacities (Table 1).
In the literature, both human and murine ES cells have well-documented differentiation and replication capacities [ 19, 20].
The viral replication capacities of GFP-PRRSV and its parental PRRSV were estimated based on the viral titers in Marc-145 and PAMs.
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Although NYVAC-C7L-Luc was able to replicate to limited extent after 3 days of infection, its replication capacity was restricted, probably because it still lacks other host range and immunomodulatory genes in its genome and as a consequence the virus was clarified faster than WR-Luc.
Researchers have speculated that declines in HIV replication capacity and virulence may be attributed to not only rapid adaptation to protective variants but also increasing use of antiretroviral treatments.
In Botswana, for instance, where HIV has adapted to overcome the protective effects of the HLA-B*57 variant, seroprevalence (the frequency of HIV infection) is increased but viral replication capacity is reduced.
However, the remaining cells did not lose their replication capacity [17].
Measuring hepatitis C virus (HCV) replication capacity utilizing primarily sub-genomic reporter constructs is limited.
The replication capacity of this CRAd is driven by a 0.5-Kb SPARC promoter fragment (named F512).
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