The role of respiratory viruses in transmission of Streptococcus pneumoniae is poorly understood. Key questions such as which serotypes are most fit for transmission and disease, and whether influenza virus alters these parameters in a serotype specific manner have not been adequately studied. In a novel model of ferret transmission, we demonstrated that prior infection with influenza virus of donors enhanced pneumococcal transmission and disease. Nasal wash bacterial titers, the incidence of mucosal and invasive disease, and the percentage of contacts infected were all increased. Viral infection of contact ferrets increased their susceptibility to acquisition both in terms of percentage infected and distance over which they could acquire infection. These influenza mediated effects on colonization, transmission and disease were pneumococcal strain dependent. Overall, these data argue that human studies of the relationship between respiratory viral infections, acquisition of pneumococci, and development of disease need further study to be better understood.

Superinfections from Staphylococcus aureus following influenza are an increasing concern. We assessed several laboratory and clinical strains in a mouse coinfection model with influenza virus. A methicillin-resistant USA300 clone and several recent clinical strains from patients with necrotizing pneumonia caused high mortality following influenza virus infection in mice. Both viral and bacterial lung titers were enhanced during coinfections compared with single infections. However, differences in titers did not correspond with differences in disease outcomes in a comparison of superinfections from a highly pathogenic strain with those from a poorly pathogenic strain. These strains did differ, however, in expression of Panton-Valentine leukocidin and in the degree of inflammatory lung damage each engendered. The viral cytotoxin PB1-F2 contributed to the negative outcomes. These data suggest that additional study of specific bacterial virulence factors involved in the pathogenesis of inflammation and lung damage during coinfections is needed.

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The segmented genome of influenza B virus allows exchange of gene segments between cocirculating strains. Through this process of reassortment, diversity is generated by the mixing of genes between viruses that differ in one or more gene segments. Phylogenetic and evolutionary analyses of all 11 genes of 31 influenza B viruses isolated from 1979 to 2003 were used to study the evolution of whole genomes. All 11 genes diverged into two new lineages prior to 1987. All genes except the NS1 gene were undergoing linear evolution, although the rate of evolution and the degree to which nucleotide changes translated into amino acid changes varied between lineages and by gene. Frequent reassortment generated 14 different genotypes distinct from the gene constellation of viruses circulating prior to 1979. Multiple genotypes cocirculated in some locations, and a sequence of reassortment events over time could not be established. The surprising diversity of the viruses, unrestricted mixing of lineages, and lack of evidence for coevolution of gene segments do not support the hypothesis that the reassortment process is driven by selection for functional differences.

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