Victoria Gregory

TL;DR: The evolution of influenza viruses results in recurrent annual epidemics of disease that are caused by progressive antigenic drift of influenza A and B viruses due to the mutability of the RNA genome and infrequent but severe pandemics caused by the emergence of novel influenza A subtypes to which the population has little immunity as mentioned in this paper.

TL;DR: Previous approaches to antigenic cartography are extended, and simultaneously characterize antigenic and genetic evolution by modeling the diffusion of antigenic phenotype over a shared virus phylogeny, and it is shown that A/H3N2 evolves faster and in a more punctuated fashion than other influenza lineages.

TL;DR: It is shown that 222G variants infected a higher proportion of ciliated cells in cultures of human airway epithelium than did viruses with 222D or 222E, which targeted mainly nonciliated cells.

TL;DR: Although analyses of the surface protein genes of the H5N1 viruses from this outbreak did not provide immediate answers regarding the molecular basis for virulence, the analyses provided clues to potentially important areas of the genes worth further investigation.

TL;DR: The inhibition of NA-dependent agglutination by the inclusion of oseltamivir carboxylate in the assay was effective in restoring the anti-HA specificity of the hemagglutination inhibition (HI) assay for monitoring antigenic changes in HA.