Evaluation of alternative respiratory syndromes for specific syndromic surveillance of influenza and respiratory syncytial virus: a time series analysis

<p>Abstract</p> <p>Background</p> <p>Syndromic surveillance is increasingly being evaluated for its potential for early warning of increased disease activity in the population. However, interpretation is hampered by the difficulty of attributing a causative pathogen. We described the temporal relationship between laboratory counts of influenza and respiratory syncytial virus (RSV) detection and alternative groupings of Emergency Department (ED) respiratory diagnoses.</p> <p>Methods</p> <p>ED and laboratory data were obtained for the south-eastern area of Sydney, NSW for the period 1 June 2001 - 1 December 2006. Counts of ED visits and laboratory confirmed positive RSV and influenza cases were aggregated by week. Semi-parametric generalized additive models (GAM) were used to determine the association between the incidence of RSV and influenza and the incidence of respiratory syndrome ED presentations while controlling for temporal confounders.</p> <p>Results</p> <p>For every additional RSV laboratory count, ED diagnoses of bronchiolitis increased by 3.1% (95%CI: 2.7%-3.5%) in the same week. For every additional influenza laboratory count, ED diagnoses of influenza-like illness increased by 4.7% (95%CI: 4.2%-5.2%) one week earlier.</p> <p>Conclusion</p> <p>In this study, large increases in ED diagnoses of bronchiolitis and influenza-like illness were independent and proxy indicators for RSV and influenza activity, respectively.</p

Respiratory syncytial virus impairs T cell activation by preventing synapse assembly with dendritic cells

Respiratory syncytial virus (RSV) infection is one of the leading causes of infant hospitalization and a major health and economic burden worldwide. Infection with this virus induces an exacerbated innate proinflammatory immune response characterized by abundant immune cell infiltration into the airways and lung tissue damage. RSV also impairs the induction of an adequate adaptive T cell immune response, which favors virus pathogenesis. Unfortunately, to date there are no efficient vaccines against this virus. Recent in vitro and in vivo studies suggest that RSV infection can prevent T cell activation, a phenomenon attributed in part to cytokines and chemokines secreted by RSV-infected cells. Efficient immunity against viruses is promoted by dendritic cells (DCs), professional antigen-presenting cells, that prime antigen-specific helper and cytotoxic T cells. Therefore, it would be to the advantage of RSV to impair DC function and prevent the induction of T cell immunity. Here, we show that, although RSV infection induces maturation of murine DCs, these cells are rendered unable to activate antigen-specific T cells. Inhibition of T cell activation by RSV was observed independently of the type of TCR ligand on the DC surface and applied to cognate-, allo-, and superantigen stimulation. As a result of exposure to RSV-infected DCs, T cells became unresponsive to subsequent TCR engagement. RSV-mediated impairment in T cell activation required DC-T cell contact and involved inhibition of immunological synapse assembly among these cells. Our data suggest that impairment of immunological synapse could contribute to RSV pathogenesis by evading adaptive immunity and reducing T cell-mediated virus clearance

Metastatic niche functions and therapeutic opportunities

Metastasis is an inefficient process, especially during colonization at a distant organ. This bottleneck underlies the importance of the metastatic niche for seeding and outgrowth of metastases. Here, we classify the common functions of different metastatic niches: anchorage, survival support, protection from external insults, licensing proliferation and outgrowth. We highlight the emerging role of the metastatic niche in maintaining cancer stemness and promoting immune evasion, and discuss therapeutic opportunities against the metastatic niche