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Modulation of infected host cells by intracellular pathogens is a prerequisite for successful establishment of infection.
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Despite the progresses achieved in the last years, more studies on the role of iron in the parasite development and on modulation of iron metabolism in infected hosts are required before translation of this knowledge into effective treatments.
Since changes in cell shape are generally related to alterations in the organization of the cytoskeleton, we have decided to investigate possible modulations in the actin network of infected neurons.
Thus, it may be that modulation of the function and maturation of infected DCs, rather than inhibition of antigen presentation per se, determines the relative importance of direct versus cross-priming of CD8+ T cells in MCMV infection.
To investigate whether the modulation of DC function following uptake of infected neutrophils is associated with Mer receptor signaling, Mer−/− or C57BL/6 (wt) mice were used as a source of bone marrow-derived DCs.
Mechanistic studies using rapamycin recently revealed that the mTOR pathway is critical for modulation of HCMV late genes in infected macrophages.
This facilitates its interaction with several kinases and adaptor proteins in the endocytic machinery, leading to the modulation of several signaling cascades in infected cells [ 3].
Figure 7: Proteomic analysis reveals the strong modulation of protein levels in PstAvrB-infected GC plants compared to wild-type controls.
A recent study of microRNA signature of prion-induced neurodegeneration [64] has shown that EGR1, E2F1 and MAZ might be also implicated in the putative deregulation of immune response related genes by miRNAs via modulation of transcriptional regulators in scrapie-infected mice.
Although those studies provided an important insight into modulation of autophagy within HIV-1-infected cells, the fact that only a fraction of cells in vivo are estimated to be infected stresses the importance of determining whether HIV-1 inhibits autophagy in bystander cells.
This may contribute to the suppression of the well-established defense response system of Anopheles vectors in turn leading to the increased infectivity and modulation of parasite gene expression [7] observed in chloroquine-treated infected mosquitoes.
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