The immune response to respiratory syncytial virus (RSV) infection has fascinated and frustrated investigators for decades. After adverse responses to early attempts at vaccination, it became popularly held that disease following infection was related to overly aggressive immune responses. However, recent data illustrate that severe forms of disease are related to inadequate, rather than hyperresponsive, adaptive immune reactions. Thus, recovery from primary (and perhaps later) RSV infection is dependent on the quality of innate immune responses. These findings should have enormous significance to the development of vaccines and antiviral compounds.
[Show abstract][Hide abstract] ABSTRACT: To determine the burden of norovirus infections in children stools from a longitudinal community cohort were evaluated using reverse transcription polymerase chain reaction. Norovirus was detected in 21.3% of diarrheal and 8.0% of nondiarrheal stools (P < 0.01). Norovirus diarrhea was highly associated with age and the odds ratio for norovirus diarrhea fell by 2.8% per month (OR = 0.97, 95% CI: 0.95-0.99). Norovirus seems to be an important etiology of community acquired diarrhea in this study population.
[Show abstract][Hide abstract] ABSTRACT: Previously healthy children hospitalized with respiratory syncytial virus (RSV) received motavizumab (3, 15, or 30 mg/kg intravenously), an RSV-specific monoclonal antibody, or placebo. Safety, tolerability, motavizumab concentrations, and immunogenicity were assessed. Cultivatable RSV in the upper respiratory tract was significantly reduced with motavizumab compared with placebo day 1 post-treatment. No adverse events were considered motavizumab-related by site investigators.
[Show abstract][Hide abstract] ABSTRACT: Respiratory syncytial virus (RSV) is a common respiratory viral infection in children which is associated with immune dysregulation
and subsequent induction and exacerbations of asthma. We recently reported that treatment of primary human epithelial cells
(PHBE cells) with transforming growth factor β (TGF-β) enhanced RSV replication. Here, we report that the enhancement of RSV
replication is mediated by induction of cell cycle arrest. These data were confirmed by using pharmacologic inhibitors of
cell cycle progression, which significantly enhanced RSV replication. Our data also showed that RSV infection alone resulted
in cell cycle arrest in A549 and PHBE cells. Interestingly, our data showed that RSV infection induced the expression of TGF-β
in epithelial cells. Blocking of TGF-β with anti-TGF-β antibody or use of a specific TGF-β receptor signaling inhibitor resulted
in rescue of the RSV-induced cell cycle arrest, suggesting an autocrine mechanism. Collectively, our data demonstrate that
RSV regulates the cell cycle through TGF-β in order to enhance its replication. These findings identify a novel pathway for
upregulation of virus replication and suggest a plausible mechanism for association of RSV with immune dysregulation and asthma.
Journal of Virology 09/2009; 83(23):12424-31. DOI:10.1128/JVI.00806-09 · 4.44 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.