The goal was to determine which virus removal mechanisms (retention by clean backwashed membrane, retention by cake layer, attachment to biomass, and inactivation) were most impacted by differences in the virus surface properties.
These differential effects may be explained by differences in the virus-mediated upregulation of inflammatory cytokine production, since the potentiation of cytokine production in infected human PBMCs has been shown to be associated to CVB4 infectivity.
However, concerns about the methodological quality of the controlled before and after studies suggest that the benefits may have been caused by differences in the populations, especially in virus infection rates.
RIDT sensitivity is greatly influenced by differences in the level of virus shedding between children and adults, making studies difficult to compare (3 ).
By using all phylogenetic methods, we found differences in virus clustering.
Non-genetic differences in virus infectivity were minimized by growing the viruses simultaneously under the same conditions and exposing mosquitoes to very similar blood meal titers (Table 1).
Observed differences in selective pressure could not be accounted for by differences in the pathogenicity of the virus, or the taxonomic order of the avian host from which it was sampled.
Epidemic dynamics may be influenced by ecological factors that influence habitat use by waterfowl species, species differences in susceptibility, age- and species-related differences in virus shedding, environmental conditions that influence virus persistence in wetlands [10], and immunity (or cross-immunity) from a previous exposure to influenza viruses [11].
Differences in virus evolution may explain virulence heterogeneity.
Genetic differences among subtypes may result in differences in virus virulence and epidemic potential (13 ).
