We are analyzing https://link.springer.com/article/10.1007/s13311-016-0450-6.

Title:
Exosomes in Viral Disease | Neurotherapeutics
Description:
Viruses have evolved many mechanisms by which to evade and subvert the immune system to ensure survival and persistence. However, for each method undertaken by the immune system for pathogen removal, there is a counteracting mechanism utilized by pathogens. The new and emerging role of microvesicles in immune intercellular communication and function is no different. Viruses across many different families have evolved to insert viral components in exosomes, a subtype of microvesicle, with many varying downstream effects. When assessed cumulatively, viral antigens in exosomes increase persistence through cloaking viral genomes, decoying the immune system, and even by increasing viral infection in uninfected cells. Exosomes therefore represent a source of viral antigen that can be used as a biomarker for disease and targeted for therapy in the control and eradication of these disorders. With the rise in the persistence of new and reemerging viruses like Ebola and Zika, exploring the role of exosomes become more important than ever.
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Keywords {🔍}

pubmed, exosomes, article, google, scholar, cas, cells, viral, virus, central, cell, infection, hiv, viruses, human, immune, exosome, vesicles, proteins, exosomal, pathway, extracellular, tax, role, shown, membrane, biol, protein, system, infected, virol, disease, dendritic, release, found, mechanism, important, type, endosomal, escrt, rab, particles, raba, zika, cellular, plasma, htlv, ebv, communication, shed,

Topics {✒️}

gov/zika/hc-providers/qa-pregnant-women myelopathy/tropical spastic paraparesis epstein-barr virus-infected cells gov/ct2/show/nct02147418 adult t-cell leukemia trigger guillain-barre syndrome cd4+ t-cell depletion lymphotropic virus type homogenous cup-shaped appearance viral oncogenes e6/e7 van der sluijs extracellular vesicle uptake epstein-barr virus latency tcr/cd3/zeta complex long-term infection favor tetraspanin-enriched microdomains reveals autophagy/multivesicular body pathways van eijndhoven ma central nervous system directing ubiquitin-labeled proteins t-cell immunoglobulin cytomegalovirus-mediated cis-infection increase t-cell apoptosis related subjects direct cell–cell contact target cell trans-infection campbell pe human leukocyte antigen-dr ebv-negative skin lesions efficient receptor-independent uptake hsv1-infected cells express hhv-6b-infected cells dendritic cell-derived exosomes hpv-positive tumor cells respiratory syncytial virus sampey gc b-cell exosome proteins epstein–barr virus epstein-barr virus capture mhc-peptide complexes v-snare proteins involved human papilloma virus de castro ro ali sa privacy choices/manage cookies herpes virus transcription t-cell activation including nasopharyngeal sarcomas fraile-ramos human herpes virus

Questions {❓}

Exosomes: cell garbage can, therapeutic carrier, or trojan horse?
HIV and mature dendritic cells: Trojan exosomes riding the Trojan horse?
Oligodendrocytes secrete exosomes containing major myelin and stress-protective proteins: Trophic support for axons?
Thus, the question becomes: Does their ability to manipulate exosomal contents allow these viruses to establish latency, or does long-term infection favor the ability to isolate exosomes while transient infections have been largely ignored due to the belief that immune clearance negates the risk of exosomes?

Schema {🗺️}

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         headline:Exosomes in Viral Disease
         description:Viruses have evolved many mechanisms by which to evade and subvert the immune system to ensure survival and persistence. However, for each method undertaken by the immune system for pathogen removal, there is a counteracting mechanism utilized by pathogens. The new and emerging role of microvesicles in immune intercellular communication and function is no different. Viruses across many different families have evolved to insert viral components in exosomes, a subtype of microvesicle, with many varying downstream effects. When assessed cumulatively, viral antigens in exosomes increase persistence through cloaking viral genomes, decoying the immune system, and even by increasing viral infection in uninfected cells. Exosomes therefore represent a source of viral antigen that can be used as a biomarker for disease and targeted for therapy in the control and eradication of these disorders. With the rise in the persistence of new and reemerging viruses like Ebola and Zika, exploring the role of exosomes become more important than ever.
         datePublished:2016-06-20T00:00:00Z
         dateModified:2016-06-20T00:00:00Z
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      headline:Exosomes in Viral Disease
      description:Viruses have evolved many mechanisms by which to evade and subvert the immune system to ensure survival and persistence. However, for each method undertaken by the immune system for pathogen removal, there is a counteracting mechanism utilized by pathogens. The new and emerging role of microvesicles in immune intercellular communication and function is no different. Viruses across many different families have evolved to insert viral components in exosomes, a subtype of microvesicle, with many varying downstream effects. When assessed cumulatively, viral antigens in exosomes increase persistence through cloaking viral genomes, decoying the immune system, and even by increasing viral infection in uninfected cells. Exosomes therefore represent a source of viral antigen that can be used as a biomarker for disease and targeted for therapy in the control and eradication of these disorders. With the rise in the persistence of new and reemerging viruses like Ebola and Zika, exploring the role of exosomes become more important than ever.
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      name:Department of Pathology Molecular and Cellular Basis of Disease Graduate Program, University of Virginia School of Medicine, Charlottesville, USA
      name:George Mason University, National Center for Biodefense and Infectious Disease, Laboratory of Molecular Virology, Manassas, USA
      name:National Institutes of Health, National Institute of Neurological Disorders and Stroke, Neuroimmunology Branch, Viral Immunology Section, Bethesda, USA

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