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Most significantly, they found that there were substantial genetic differences in the viruses taken from human and mosquito blood samples.
The higher rates of seropositivity in the studies following the 1997 outbreak may reflect the genetic differences in the viruses circulating now compared to the 1997 virus, which may have been more adaptable to human infection [59].
This difference in transmissibility could have resulted from innate differences in the viruses themselves or from a level of immunity from past infection with the seasonal strain.
This confirms our previous observation in EX-CELL Vero SFM, that the inherent differences in the viruses, such as the deletion of the NS1 gene, may be the primary factor resulting in the different virus titres.
Years later, extensive characterization of HA and NA antigens of the 1943 and 1947 viruses and comparison of their nucleotide and amino acid sequences showed marked differences in the viruses isolated in these 2 years; studies in a mouse model also showed that the 1943 vaccine afforded no protection to the 1947 virus challenge (24 ).
We speculate that this may be largely due to differences in the viruses, especially the NS1 deletion, since it was known that the NS1 protein in infected cells interacts with host cell gene expression and cellular protein regulation including interferon mediated antiviral responses [ 11, 60, 61].
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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.
As a result, the differences observed between high and partial load are believed to relate to differences in exhaust composition and not to differences in the virus.
These factors may lead to an underestimation of the extent to which clinical outcome of patients varies because of differences in the virus subtype(s) present.
We speculated that the earlier age of infection in Guinea Bissau might be explained by a higher infectivity — comparable to that in temperate climates, due to genetic differences in the virus or its environment.
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.
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