Number of circulating CD 73-expressing lymphocytes correlates with survival after cardiac arrest.

Background Patients resuscitated from cardiac arrest ( CA ) have highly variable neurological, circulatory, and systemic ischemia-reperfusion injuries. After the initial hypoxic-ischemic insult, a cascade of immune and inflammatory responses develops and is often fatal. The role of the immune response in pathophysiological characteristics and recovery is not well understood. We studied immune cell activity and its association with outcomes in a cohort of CA survivors. Methods and Results After informed consent, we collected blood samples at intervals over a week after resuscitation from CA . We examined the expression of CD 39 and CD 73 (alias 5\u27-nucleotidase), production of tumor necrosis factor-α, generation of reactive oxygen species, and secretion of vascular endothelial growth factor by circulating myeloid and lymphoid cells, in comparison to cells obtained from control subjects before coronary artery bypass grafting surgery. The number of circulating total and CD 73-expressing lymphocytes correlated with survival after CA . Incubation of immune cells, obtained from post- CA subjects, with AMP , a substrate for CD 73, resulted in inhibition of tumor necrosis factor-α production and generation of reactive oxygen species. This effect was blocked by adenosine 5\u27-(α, β-methylene) diphosphate, a specific inhibitor of CD 73 and ZM 241385, an A2 adenosine receptor antagonist. We also found that AMP -dependent activation of CD 73 induces production of vascular endothelial growth factor. Conclusions CD 73-expressing lymphocytes mediate cellular protection from inflammation after CA through inhibition of proinflammatory activation of myeloid cells and promotion of vascular endothelial growth factor secretion. The contribution of CD 73 lymphocytes in the regulation of acute inflammation and tissue injury after CA warrants further study

How much can diptera-borne viruses persist over unfavourable seasons

Diptera are vectors of major human and animal pathogens worldwide, such as dengue, West-Nile or bluetongue viruses. In seasonal environments, vector-borne disease occurrence varies with the seasonal variations of vector abundance. We aimed at understanding how diptera-borne viruses can persist for years under seasonal climates while vectors overwinter, which should stop pathogen transmission during winter. Modeling is a relevant integrative approach for investigating the large panel of persistence mechanisms evidenced through experimental and observational studies on specific biological systems. Inter-seasonal persistence of virus may occur in hosts due to viremia duration, chronic infection, or vertical transmission, in vector resistance stages, and due to a low continuous transmission in winter. Using a generic stochastic modeling framework, we determine the parameter ranges under which virus persistence could occur via these different mechanisms. The parameter ranges vary according to the host demographic regime: for a high host population turnover, persistence increases with the mechanism parameter, whereas for a low turnover, persistence is maximal for an optimal range of parameter. Persistence in hosts due to long viremia duration in a few hosts or due to vertical transmission is an effective strategy for the virus to overwinter. Unexpectedly, a low continuous transmission during winter does not give rise to certain persistence, persistence barely occurring for a low turnover of the susceptible population. We propose a generic framework adaptable to most diptera-borne diseases. This framework allows ones to assess the plausibility of each persistence mechanism in real epidemiological situations and to compare the range of parameter values theoretically allowing persistence with the range of values determined experimentally