Fifty infants younger than six months, hospitalized for infection with respiratory syncytial virus (RSV), were studied by examination of serial samples of nasal secretion. Secretory neutralizing activity was measured by plaque reduction and secretory antibody by indirect fluorescence using conjugated antiserum to human IgA, IgG, or IgM. Secretory neutralizing activity during infection rose or fell fourfold with approximately equal frequency (20% and 26%, respectively). In contrast, levels of IgA antibody to RSV in secretions rose fourfold in 56%--65% of the infants and fell in none. The frequency of such rises in titer of antibody was directly related to age. In individual secretions the correlation between neutralizing activity and IgA antibody to RSV was poor: neutralizing activity was often found in the absence of detectable antibody, and IgA antibody to RSV was often nonneutralizing. Nevertheless, the development of IgA antibody to RSV correlated in time with the disappearance of virus from the respiratory tract. The timing of this secretory response is consistent with the hypothesis that antibody contributes significantly to cure of infection.

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An enzyme-linked immunosorbent assay (ELISA) was developed for detection of respiratory syncytial virus (RSV) in nasal secretions from infants with respiratory disease. RSV was detected in 23 of 29 secretions positive for RSV by tissue culture and in one of 36 samples negative for RSV by tissue culture. The ELISA was a simple rapid, and surprisingly sensitive test for identification of RSV infection in infants.

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Background: Macrophages participate in all stages of the inflammatory response, and the excessive release of inflammatory mediators and other cytokines synthesized and secreted by macrophages is fundamentally linked to an uncontrolled inflammatory response. The zinc finger 667 (ZNF667) protein, a novel DNAbinding protein, has been shown to play a vital role in oxidative stress. However, none of the target genes in macrophages or the potential roles of ZNF667 have been elucidated to date. Objectives: The present study was designed to investigate the effects of ZNF667 on LPS-induced inflammation in macrophages. Methods: The RAW264.7 macrophage cell line was selected as a model system. Inflammatory response-related gene expression levels and phosphorylation levels of PI3K, AKT, and mTOR were detected in LPS-treated macrophages via RT-PCR and western blotting, respectively. Results: We found that LPS resulted in the up-regulation of ZNF667 in macrophages and a peak response in ZNF667 protein expression levels when used at a concentration of 100 ng/mL. ZNF667 overexpression significantly inhibited the LPS-induced up-regulation of iNOS, and IL-1β mRNA and protein expression levels, together with the secretion of IL-1β, IL-6, and TNF-α. ZNF667 overexpression also inhibited PI3K, AKT, and mTOR hyperphosphorylation and had no effect on the phosphorylation of NF-κB p65, ERK1/2, MAPK p38, and the transcriptional activity of NF-κB in macrophages. The up-regulation of ZNF667 inhibited the levels of expression of HK2 and PFKFB3, glucose consumption, and lactate production in LPS-stimulated macrophages. The up-regulation of mRNA levels of LPS-induced glycolytic genes HK2 and PFKFB3 and the increased mRNA expression of pro-inflammatory cytokines (IL-1β and iNOS) were abolished by hexokinase inhibitor 2-DG in ZNF667-deficient macrophages. Meanwhile, glucose consumption and lactate production were abrogated in macrophages when cells were treated with the specific mTOR inhibitor RPM. Conclusion: Our results demonstrate that ZNF667 suppressed LPS-stimulated RAW264.7 macrophage inflammation by regulating mTOR-dependent aerobic glycolysis.