The PCR target genes were: 16S rRNA for total bacterial load [ 28], autolysin (lytA) for S. pneumoniae load [ 29], protein D (hpd) for H. influenzae load [ 3], and the outer membrane protein (copB) for M. catarrhalis load [ 30].
H. influenzae load was significantly elevated in the presence of HPyV, HCoV and any study virus, and linear regression revealed that the loads of M.catarrhalis and H. influenzae were higher with detection of multiple viruses (Table 2).
However, this assumption could have been violated in some instances, for example if influenza viral load varied substantially among persons and higher viral loads increased the likelihood of detection by both systems.
An early preventive treatment of upper respiratory tract viral infection with a mild and nontoxic antipathogenic agent like cod trypsin may be effective in reducing the RSV and influenza viral load and possibly prevent bacterial coinfection.
These serial dilutions were used to establish the relationship between influenza viral load determined by ResPlex III or by RRT-PCR (i.e., between TCID50/mL and viral cDNA copies), since there is no international standard for influenza A and B viral RNA.
Multivariate regression analysis identified qPCR H influenzae bacterial load and CFU as independent predictors of sputum TNF-α and IL-1β (H influenzae, β = 0.38 and 0.32 for TNF-α and IL-1β, respectively; and CFU, β = 0.36 and 0.31, respectively) (e-Table 4).
Neither pandemic nor seasonal influenza viral loads correlated with clinical severity of illness.
However, we have demonstrated a positive association between symptoms and H influenzae bacterial load.
We offer some possible explanation for these findings but note that these influenza viral loads have been measured in respiratory samples.
First, we found no significant correlation between pandemic (H1N1) 2009 or seasonal influenza viral loads and clinical severity of illness (Table 2).
