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Background: The recent West African Ebola virus disease (EVD) outbreak had catastrophic impact on populations, health care systems and economies of the affected countries. Somatic symptoms have been reported to persist long beyond the acute infection. This review was conducted to provide an overview on neuro- and socio-psychological long-term sequelae of EVD survivors., Methods: Utilizing Pubmed and PsycInfo databases, a systematic review prepared according to PRISMA guidelines. Only studies reporting quantitative data on neuropsychological sequelae three weeks or later after discharge from the Ebola-treating unit were included. Pooled proportions of common outcomes were calculated., Results: In total, 224 papers were identified, of which 10 were included. Depression, insomnia, fatigue, anxiety and post-traumatic stress were common sequelae in EVD survivors. However, data from high-quality studies were scarce., Conclusions: EVD survivors have been thought to commonly face neuropsychological long-term sequelae. Methodological drawbacks and heterogeneity of current studies limit conclusions of the impact and magnitude of such sequelae. We advocate the preparation of a prospective, controlled cohort study protocol in preparation for a future outbreak., (Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The effect of the cyclooxygenase inhibitors, indomethacin and diclofenac, and of PGE2 on either resting or stimulated macrophages was investigated. Peritoneal macrophages were obtained from untreated mice and cultured for 10 days. Macrophage activation was induced by zymosan phagocytosis and was monitored by testing for plasminogen activator secretion and the cellular levels of lactate dehydrogenase, beta-glucuronidase and alkaline phosphodiesterase I. It was found that cyclooxygenase inhibitors activate resting macrophages and enhance the degree of activation obtained after zymosan phagocytosis. Addition of exogenous PGE2, on the other hand, had the opposite effect, it suppressed activation induced either by cyclooxygenase inhibitors, phagocytosis or a combination of both. Cyclooxygenase inhibitors and PGE2 did not affect the hexose monophosphate shunt activity of resting macrophages and had only a minor effect on the respiratory burst occurring during zymosan phagocytosis. It appears, therefore, that the observed changes in the state of activation of the macrophages are not related to hexose monophosphate shunt activity. The described effects suggest that PGE2 and possibly other cyclooxygenase products may function as inhibitory feed-back regulators of macrophage activation.