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Interferons (IFN) belong to the family of cytokines and have been described first in the late 1950s as an inhibitory factor of viral replication. Since then, the impact of interferon has been greatly expanded and its function comprises a role not only in different types of infection, cancer and autoimmunity but importantly also in immunehomeostasis. IFN have important anti-viral effects but it is becoming more and more evident that they are true immunomodulators and have an important impact on the development and maintenance of innate and adaptive immunity.

Medicine --- Immunology --- interferons --- IFN --- immunehomeostasis --- autoimmunity --- mmunomodulators

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Successful containment of an infection is dependent on both innate and adaptive immune response. Cytokines are essential effectors of both of these systems. In particular, type I interferons (IFN-I) are important components of early innate immunity against an infection. However, the production of IFN-I could serve as a double edge sword, either containing an infection or enhancing susceptibility. For example, IFN-I, which is essential for early containment of viral infections, has been shown to be detrimental to the host during bacterial infections. In fact, recent significant reports have shown that influenza virus induced IFN-I responses can enhance the host susceptibility to secondary bacterial infections. These recent reports highlight the expanding immunoregulatory role of IFN-I in the host immunity. With these recent findings in mind, the aim of this research topic is to welcome novel data, opinion and literature reviews on the newly identified dual functions of IFN-I. This research topic wills focus on the following areas of IFN-I: 1) a detrimental role of IFN-I during primary bacterial infection; 2) a detrimental role of viral infection induced IFN-I during secondary bacterial infections; 3) evolutionary pressure that drove detrimental IFN-I response during primary bacterial infection; and 4) does benefit of IFN-I responses during primary viral infections outweigh the adverse consequences of IFN-I mediated enhanced susceptibility to secondary bacterial infections.

Autoimmunity --- adjuvant --- bacterial and viral infections --- Vaccine --- type I IFN

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

interferon --- type III IFNs --- barrier --- inflammation --- IFN lambda

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Endocrine and immune parameters, namely glucocorticoid receptors (GcR) and IFN-gamma production in peripheral blood mononuclear cells (PBMC), and corticosterone in plasma, were studied in groups of four male rabbits observed in seminatural conditions in relation to agonistic behaviour and to seasonal variations. These parameters were selected on the basis of the findings that the presence of GcR in PBMC gives an indication of the in vivo biological effects of glucocorticoids and that PBMC cytokine production and plasma corticosterone are related to social behaviour. The frequency of active and passive behaviours was used to rank the animals. Seasonal variations were present for agonistic behaviours (Attack, Follow, Chase) and For plasma corticosterone, which were significantly higher in winter. IFN-gamma production in PBMC was increased after social interactions in both seasons, while plasma corticosterone was increased only in winter: GcR capacity in PBMC was decreased after social interactions. The results indicate that social and physical environmental factors are correlated with immune-endocrine functions

Agonistic behaviour,seasonal variation,corticosterone,glucocorticoid receptors,ifn-gamma production,rabbit. --- Agonistic behaviour. --- Agonistic. --- Animal. --- Animals. --- Behavior. --- Behaviour. --- Blood mononuclear-cells. --- Blood. --- Corticosterone. --- Dominance. --- Endocrine. --- Frequency. --- Function. --- Glucocorticoid receptors. --- Glucocorticoid. --- Glucocorticoids. --- Group. --- Hippocampal electrical-activity. --- Immune. --- Interaction. --- Interactions. --- Invivo. --- Male. --- Parameters. --- Physical. --- Pituitary. --- Plasma corticosterone. --- Plasma-corticosterone. --- Plasma. --- Production. --- Rabbit. --- Rabbits. --- Rank. --- Receptor. --- Receptors. --- Release. --- Responses. --- Season. --- Seasonal variation. --- Social behaviour. --- Social interaction. --- Social interactions. --- Social-interaction. --- Social. --- Stress. --- Variation.

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Zika virus (ZIKV), one of the flavivirus family members transmitted by mosquitos, was declared a Public Health Emergency of International Concern by the WHO in February 2016 because of clusters of newborn microcephaly cases and other neurological disorders in Brazil. Most ZIKV infections result in a self-limited flu-like febrile disease, however, if contracted during pregnancy, the virus can also infect fetuses and cause a spectrum of birth defects known as congenital Zika syndrome. To date, no vaccines or antiviral drugs are licensed for ZIKV, and the virus has spread and become endemic to many tropical and sub-tropical countries. Included in this book are thirteen reports addressing diverse aspects of ZIKV–host interactions. These studies range from basic science to clinical research. It is expected that findings from these studies will contribute to a better understanding of the host cells interacting with ZIKV, and may serve as the basis for new diagnostics, antiviral therapies, and vaccine design.

Research & information: general --- Biology, life sciences --- Zika virus --- peroxisomes --- innate immune response --- interferon --- astrocytes --- fetal brain --- zika virus --- flaviviruses --- T cells --- host-pathogen interactions --- flavivirus --- tight junctions --- claudins --- ZO-1 --- blood-placental barrier --- placenta --- apoptosis --- viral replication --- Bcl-2 protein family --- ZIKV --- virus host interactions --- pathogenesis --- MR766 --- guinea pig --- subcutaneous --- vaginal --- sexual transmission --- virus transmission --- envelope protein --- glycosylation --- fusion loop --- viral fusion --- cell entry --- NS5 protein --- nuclear localization --- inflammation --- innate immunity --- extracellular vesicles --- cellular communication --- C6/36 cells --- human monocytes --- endothelial vascular cells --- protein–protein interaction --- non-structural viral proteins --- network --- JAK/STAT --- cytokine --- West Nile virus --- HSP90 --- NS5 --- virus–host interactions --- anti-viral signaling --- immune response --- inflammatory mediator --- Sertoli cells --- Leydig cells --- ZIKA virus --- arboviruses --- infertility --- IFN --- RIG-I --- MDA5 --- IFNAR1 --- zika --- host --- cell death --- peroxisome --- mosquito --- tight junction --- Zika virus --- peroxisomes --- innate immune response --- interferon --- astrocytes --- fetal brain --- zika virus --- flaviviruses --- T cells --- host-pathogen interactions --- flavivirus --- tight junctions --- claudins --- ZO-1 --- blood-placental barrier --- placenta --- apoptosis --- viral replication --- Bcl-2 protein family --- ZIKV --- virus host interactions --- pathogenesis --- MR766 --- guinea pig --- subcutaneous --- vaginal --- sexual transmission --- virus transmission --- envelope protein --- glycosylation --- fusion loop --- viral fusion --- cell entry --- NS5 protein --- nuclear localization --- inflammation --- innate immunity --- extracellular vesicles --- cellular communication --- C6/36 cells --- human monocytes --- endothelial vascular cells --- protein–protein interaction --- non-structural viral proteins --- network --- JAK/STAT --- cytokine --- West Nile virus --- HSP90 --- NS5 --- virus–host interactions --- anti-viral signaling --- immune response --- inflammatory mediator --- Sertoli cells --- Leydig cells --- ZIKA virus --- arboviruses --- infertility --- IFN --- RIG-I --- MDA5 --- IFNAR1 --- zika --- host --- cell death --- peroxisome --- mosquito --- tight junction