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Infectious diseases are associated with approximately 20% of global mortality, with viral diseases causing about one third of these deaths. Besides newly emerging and re-emerging viral infections will continue to pose a threat to human survival globally. In this case scientific advances have greatly been increased to defend against those pathogens. For example, rapid genomic sequencing, proteomics, epigenomics, nanotechnology, and other advanced tools are being applied to detect viruses at the point of care and to track their spread within human populations as well as to understand virus-host interaction and virus induced pathogenesis. From rapid identification of new viruses to prevention with vaccination and treatment with effective therapeutics, biomedical research has continuously provided tools to meet the constant threat of emerging viral pathogens. Despite these advances, each new disease brings unique challenges to scientists every year. So we must stay at the cutting edge of scientific discovery, working energetically to develop new tools to combat the ever-changing threats they pose. Our research topic highlights such advanced and new technology based virus research which definitely bolsters the researcher's ability to tackle emerging, re-emerging and stable viral pathogens. We are credulous that the papers including in the e-books will be beneficial to the experts in the field to understand the molecular, immunological, ecological and clinical aspects of the next generation researches for the prevention and control of infectious diseases caused by viruses.

virus-host interaction --- Nanobiosensor --- Technology --- Next generation --- diagnosis --- Re-emerging --- Proteomic analysis --- Virus research

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Unfolded protein response (UPR) is a cellular adaptive response for restoring endoplasmic reticulum (ER) homeostasis in response to ER stress. Perturbation of the UPR and failure to restore ER homeostasis inevitably leads to diseases. It has now become evident that perturbation of the UPR is the cause of many important human diseases such as neurodegenerative diseases, cystic fibrosis, diabetes and cancer. It has recently emerged that virus infections can trigger the UPR but the relationship between virus infections and host UPR is intriguing. On one hand, UPR is harmful to the virus and virus has developed means to subvert the UPR. On the other hand, virus exploits the host UPR to assist in its own infection, gene expression, establishment of persistence, reactivation from latency and to evade the immune response. When this delicate balance of virus-host UPR interaction is broken down, it may cause diseases. This is particularly challenging for viruses that establish a chronic infection to maintain this balance. Each virus interacts with the host UPR in a different way to suit their life style and how the virus interacts with the host UPR can define the characteristic of a particular virus infection. Understanding how a particular virus interacts with the host UPR may pave the way to the design of a new class of anti-viral that targets this particular pathway to skew the response towards anti-virus. This knowledge can also be translated into the clinics to help re-design oncolytic virotherapy and gene therapy. In this research topic we aimed to compile a collection of focused review articles, original research articles, commentary, opinion, hypothesis and methods to highlight the current advances in this burgeoning area of research, in an attempt to provide an in-depth understanding of how viruses interact with the host UPR, which may be beneficial to the future combat of viral and human diseases.

Virus diseases. --- Viruses. --- ERAD --- virus-host interaction --- innate immunity --- Gene Therapy --- Pathogenesis --- Endoplasmic Reticulum Stress --- Unfolded Protein Response --- Autophagy --- ERAD --- virus-host interaction --- innate immunity --- Gene Therapy --- Pathogenesis --- Endoplasmic Reticulum Stress --- Unfolded Protein Response --- Autophagy

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Unfolded protein response (UPR) is a cellular adaptive response for restoring endoplasmic reticulum (ER) homeostasis in response to ER stress. Perturbation of the UPR and failure to restore ER homeostasis inevitably leads to diseases. It has now become evident that perturbation of the UPR is the cause of many important human diseases such as neurodegenerative diseases, cystic fibrosis, diabetes and cancer. It has recently emerged that virus infections can trigger the UPR but the relationship between virus infections and host UPR is intriguing. On one hand, UPR is harmful to the virus and virus has developed means to subvert the UPR. On the other hand, virus exploits the host UPR to assist in its own infection, gene expression, establishment of persistence, reactivation from latency and to evade the immune response. When this delicate balance of virus-host UPR interaction is broken down, it may cause diseases. This is particularly challenging for viruses that establish a chronic infection to maintain this balance. Each virus interacts with the host UPR in a different way to suit their life style and how the virus interacts with the host UPR can define the characteristic of a particular virus infection. Understanding how a particular virus interacts with the host UPR may pave the way to the design of a new class of anti-viral that targets this particular pathway to skew the response towards anti-virus. This knowledge can also be translated into the clinics to help re-design oncolytic virotherapy and gene therapy. In this research topic we aimed to compile a collection of focused review articles, original research articles, commentary, opinion, hypothesis and methods to highlight the current advances in this burgeoning area of research, in an attempt to provide an in-depth understanding of how viruses interact with the host UPR, which may be beneficial to the future combat of viral and human diseases.

Virus diseases. --- Viruses. --- ERAD --- virus-host interaction --- innate immunity --- Gene Therapy --- Pathogenesis --- Endoplasmic Reticulum Stress --- Unfolded Protein Response --- Autophagy

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How complex systems theory sheds new light on the adaptive dynamics of viral populationsViruses are everywhere, infecting all sorts of living organisms, from the tiniest bacteria to the largest mammals. Many are harmful parasites, but viruses also play a major role as drivers of our evolution as a species and are essential regulators of the composition and complexity of ecosystems on a global scale. This concise book draws on complex systems theory to provide a fresh look at viral origins, populations, and evolution, and the coevolutionary dynamics of viruses and their hosts.New viruses continue to emerge that threaten people, crops, and farm animals. Viruses constantly evade our immune systems, and antiviral therapies and vaccination campaigns can be powerless against them. These unique characteristics of virus biology are a consequence of their tremendous evolutionary potential, which enables viruses to quickly adapt to any environmental challenge. Ricard Solé and Santiago Elena present a unified framework for understanding viruses as complex adaptive systems. They show how the application of complex systems theory to viral dynamics has provided new insights into the development of AIDS in patients infected with HIV-1, the emergence of new antigenic variants of the influenza A virus, and other cutting-edge advances.Essential reading for biologists, physicists, and mathematicians interested in complexity, Viruses as Complex Adaptive Systems also extends the analogy of viruses to the evolution of other replicators such as computer viruses, cancer, and languages.

Viruses. --- AIDS. --- Alan Turing. --- Arenavirus. --- Ebola. --- HIV infection. --- HIV-1 transmission. --- HIV-1. --- Hantavirus. --- RNA virus. --- SIS model. --- adaptation. --- antigenic dynamics. --- cellular origin hypothesis. --- complex adaptive system. --- computational objects. --- computer virus. --- cultural evolution. --- ecosystem regulation. --- emerging virus. --- epidemics. --- epitasis. --- evolution. --- evolutionary dynamics. --- evolutionary virology. --- fitness landscape. --- genetic diversity. --- genome reduction. --- human genome. --- human immunodeficiency virus. --- immune system. --- living organisms. --- mutation. --- mutational robustness. --- outbreaks. --- parasite. --- parasites. --- pathogenic viruses. --- population dynamics. --- populations. --- protobiont hypothesis. --- regressive hypothesis. --- replicating machine. --- scale-free networks. --- spatial dynamics. --- viral dynamics. --- viral quasispecies. --- viral symbiosis. --- viral universe. --- virus biology. --- virus dynamics. --- virus landscape. --- virus origins. --- virus-host interaction. --- viruses. --- virus-host interactions.

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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.

deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases