Sentence examples for viral blockage from inspiring English sources

Any association between deleterious Wolbachia effects and viral blockage may also not be particularly strong.

If the mechanisms involved in viral blockage, cytoplasmic incompatibility, and host fitness effects were understood, it might help in predicting likely interactions among Wolbachia effects.

These examples provide some support for a possible relationship between viral blockage, deleterious host effects and Wolbachia density, but too few strains have so far been examined.

Several authors have contrasted viral blockage (measured as survival/longevity following pathogen infection) in Wolbachia strains from Drosophila with effects on host fitness (mostly measured as longevity in the absence of the infection) and on cytoplasmic incompatibility (Table 1).

This possibility arises because a high density of Wolbachia in hosts may increase viral blockage but decrease host fitness (Chrostek et al. 2013; Sinkins 2013; Martinez et al. 2014), and such a trade-off could have driven past cycles of Wolbachia strain replacements in natural populations.

For instance, the wRi and wHa infections in D. simulans are restricted mostly to gonadal tissues (Binnington and Hoffmann 1989; Correa and Ballard 2014), have mild deleterious effects (Hoffmann et al. 1990; Turelli and Hoffmann 1995) and cause mid- to low-level viral blockage (Osborne et al. 2009).

At this point, therapeutic RNAi molecules may interact with viral RNA and blockage or reduce HIV infection.

In patients with CHB, HBV-specific CD8+ T cells were verified to have an increased propensity to express CTLA-4 strongly correlating with viral load; accordingly, blockage of CTLA-4 was able to increase the proliferation of IFN- γ-producing HBV-specific CD8+ T cells in the periphery and liver tissues.

As shown in Figure 3, in the absence of stimulation, the J-Lat 15.4 and 8.4 cells expressed no GFP, indicating a blockage of viral transcription.

In subsequent experiments, this strain was shown to have very strong blockage of viral replication and disease transmission in laboratory assays (Moreira et al. 2009).

HA induces the formation of neutralizing antibodies, creating a first blockage against viral infection [ 7, 8] and it appears that protection provided by the trivalent influenza virus vaccine is mediated primarily by anti-HA neutralizing antibodies [ 7- 9].