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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

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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

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Mitochondria are the powerhouses of cells; however, mitochondrial dysfunction causes energy depletion and cell death in a variety of diseases. Altered oxidative phosphorylation and ion homeostasis are associated with ROS production resulting from the disassembly of respiratory supercomplexes and the disruption of electron transfer chains. In pathological conditions, the dysregulation of mitochondrial homeostasis promotes Ca2+ overload in the matrix and ROS accumulation, which induces the mitochondrial permeability transition pore formation responsible for mitochondrial morphological changes linked to membrane dynamics, and ultimately, cell death. Finally, studies on the impaired mitochondrial bioenergetics in pathology could provide molecular tools to counteract diseases associated with mitochondrial dysfunction.

Research & information: general --- Biology, life sciences --- Biochemistry --- aging heart --- Bcl-2 family --- mitochondria --- programmed cell death --- fatty acid oxidation --- palmitate --- oleate --- m.3243A&gt --- G mutation --- MT-ATP6 --- m.8909T&gt --- C --- ATP synthase --- nephropathy --- oxidative phosphorylation --- mitochondrial disease --- cardiolipin --- Barth syndrome --- Sengers syndrome --- respiratory chain --- Dilated Cardiomyopathy with Ataxia --- cardiomyopathy --- mammalian complex I --- NADH dehydrogenase --- complex I assembly --- complex I structure --- complex I deficiency --- supernumerary subunits --- electron transport chain --- mitochondrial dysfunction --- Leigh syndrome --- mitochondrial diseases --- yeast --- Saccharomyces cerevisiae --- pet mutants --- pancreatic endocrine cells --- mathematical model --- cellular bioenergetics --- diabetes --- glucagon --- insulin --- exercise --- immune system --- metabolic disease --- COVID-19 --- mitochondrial dynamics --- viral infections --- MAVS --- RIG-I --- MDA5 --- innate immune response --- SARS CoV-2 --- RSV --- influenza --- respiratory supercomplexes --- ROS --- ATP synthase/hydrolase --- mitochondrial permeability transition pore --- cristae --- cellular signaling --- human disease --- mitochondrial dynamic --- cell signaling --- cancer --- respiratory complexes --- oxidative stress --- mitochondrial DNA --- MTCYB mutations --- cytochrome b --- complex III --- aging --- energy metabolism --- entorhinal cortex --- lipoxidation-derived damage --- neurodegeneration --- oxidative damage --- protein import --- respiratory complex assembly --- supercomplexes --- mitochondrial proteostasis --- heart failure --- bioenergetics --- assembly factor --- atypical myopathy --- high-resolution respirometry --- toxicity assays --- cell culture --- equine primary myoblasts --- fibroblasts --- frozen tissue --- leukocytes --- oxygen consumption --- platelets --- respirometry --- skeletal muscle