يعرض 1 - 7 نتائج من 7 نتيجة بحث عن '"Viral Structure"', وقت الاستعلام: 1.12s تنقيح النتائج
  1. 1
    دورية أكاديمية

    المصدر: Viruses, Vol 16, Iss 3, p 427 (2024)

    الوصف: The structural study of plant viruses is of great importance to reduce the damage caused by these agricultural pathogens and to support their biotechnological applications. Nowadays, X-ray crystallography, NMR spectroscopy and cryo-electron microscopy are well accepted methods to obtain the 3D protein structure with the best resolution. However, for large and complex supramolecular structures such as plant viruses, especially flexible filamentous ones, there are a number of technical limitations to resolving their native structure in solution. In addition, they do not allow us to obtain structural information about dynamics and interactions with physiological partners. For these purposes, small-angle X-ray scattering (SAXS) and atomic force microscopy (AFM) are well established. In this review, we have outlined the main principles of these two methods and demonstrated their advantages for structural studies of plant viruses of different shapes with relatively high spatial resolution. In addition, we have demonstrated the ability of AFM to obtain information on the mechanical properties of the virus particles that are inaccessible to other experimental techniques. We believe that these under-appreciated approaches, especially when used in combination, are valuable tools for studying a wide variety of helical plant viruses, many of which cannot be resolved by classical structural methods.

    وصف الملف: electronic resource

  2. 2
    دورية أكاديمية

    الوصف: Coronaviruses are a large family of zoonotic RNA viruses, whose infection can lead to mild or lethal respiratory tract disease. Severe Acute Respiratory Syndrome-Coronavirus-1 (SARS-CoV-1) first emerged in Guangdong, China in 2002 and spread to 29 countries, infecting 8089 individuals and causing 774 deaths. In 2012, Middle East Respiratory Syndrome-Coronavirus (MERS-CoV) emerged in Saudi Arabia and has spread to 27 countries, with a mortality rate of ~34%. In 2019, SARS-CoV-2 emerged and has spread to 220 countries, infecting over 100,000,000 people and causing more than 2,000,000 deaths to date. These three human coronaviruses cause diseases of varying severity. Most people develop mild, common cold-like symptoms, while some develop acute respiratory distress syndrome (ARDS). The success of all viruses, including coronaviruses, relies on their evolved abilities to evade and modulate the host anti-viral and pro-inflammatory immune responses. However, we still do not fully understand the transmission, phylogeny, epidemiology, and pathogenesis of MERS-CoV and SARS-CoV-1 and -2. Despite the rapid application of a range of therapies for SARS-CoV-2, such as convalescent plasma, remdesivir, hydroxychloroquine and type I interferon, no fully effective treatment has been determined. Remarkably, COVID-19 vaccine research and development have produced several offerings that are now been administered worldwide. Here, we summarise an up-to-date understanding of epidemiology, immunomodulation and ongoing anti-viral and immunosuppressive treatment strategies. Indeed, understanding the interplay between coronaviruses and the anti-viral immune response is crucial to identifying novel targets for therapeutic intervention, which may even prove invaluable for the control of future emerging coronavirus.

    وصف الملف: Electronic; application/pdf

  3. 3
    دورية أكاديمية

    المصدر: Viruses, Vol 13, Iss 560, p 560 (2021)

    الوصف: Coronaviruses are a large family of zoonotic RNA viruses, whose infection can lead to mild or lethal respiratory tract disease. Severe Acute Respiratory Syndrome-Coronavirus-1 (SARS-CoV-1) first emerged in Guangdong, China in 2002 and spread to 29 countries, infecting 8089 individuals and causing 774 deaths. In 2012, Middle East Respiratory Syndrome-Coronavirus (MERS-CoV) emerged in Saudi Arabia and has spread to 27 countries, with a mortality rate of ~34%. In 2019, SARS-CoV-2 emerged and has spread to 220 countries, infecting over 100,000,000 people and causing more than 2,000,000 deaths to date. These three human coronaviruses cause diseases of varying severity. Most people develop mild, common cold-like symptoms, while some develop acute respiratory distress syndrome (ARDS). The success of all viruses, including coronaviruses, relies on their evolved abilities to evade and modulate the host anti-viral and pro-inflammatory immune responses. However, we still do not fully understand the transmission, phylogeny, epidemiology, and pathogenesis of MERS-CoV and SARS-CoV-1 and -2. Despite the rapid application of a range of therapies for SARS-CoV-2, such as convalescent plasma, remdesivir, hydroxychloroquine and type I interferon, no fully effective treatment has been determined. Remarkably, COVID-19 vaccine research and development have produced several offerings that are now been administered worldwide. Here, we summarise an up-to-date understanding of epidemiology, immunomodulation and ongoing anti-viral and immunosuppressive treatment strategies. Indeed, understanding the interplay between coronaviruses and the anti-viral immune response is crucial to identifying novel targets for therapeutic intervention, which may even prove invaluable for the control of future emerging coronavirus.

  4. 4

    المساهمون: Apollo - University of Cambridge Repository, Lu, Yongxu [0000-0003-4701-5560]

    المصدر: Viruses
    Viruses, Vol 13, Iss 560, p 560 (2021)

    الوصف: Coronaviruses are a large family of zoonotic RNA viruses, whose infection can lead to mild or lethal respiratory tract disease. Severe Acute Respiratory Syndrome-Coronavirus-1 (SARS-CoV-1) first emerged in Guangdong, China in 2002 and spread to 29 countries, infecting 8089 individuals and causing 774 deaths. In 2012, Middle East Respiratory Syndrome-Coronavirus (MERS-CoV) emerged in Saudi Arabia and has spread to 27 countries, with a mortality rate of ~34%. In 2019, SARS-CoV-2 emerged and has spread to 220 countries, infecting over 100,000,000 people and causing more than 2,000,000 deaths to date. These three human coronaviruses cause diseases of varying severity. Most people develop mild, common cold-like symptoms, while some develop acute respiratory distress syndrome (ARDS). The success of all viruses, including coronaviruses, relies on their evolved abilities to evade and modulate the host anti-viral and pro-inflammatory immune responses. However, we still do not fully understand the transmission, phylogeny, epidemiology, and pathogenesis of MERS-CoV and SARS-CoV-1 and -2. Despite the rapid application of a range of therapies for SARS-CoV-2, such as convalescent plasma, remdesivir, hydroxychloroquine and type I interferon, no fully effective treatment has been determined. Remarkably, COVID-19 vaccine research and development have produced several offerings that are now been administered worldwide. Here, we summarise an up-to-date understanding of epidemiology, immunomodulation and ongoing anti-viral and immunosuppressive treatment strategies. Indeed, understanding the interplay between coronaviruses and the anti-viral immune response is crucial to identifying novel targets for therapeutic intervention, which may even prove invaluable for the control of future emerging coronavirus.

    وصف الملف: application/pdf; text/xml

  5. 5

    المصدر: Proceedings, Vol 50, Iss 116, p 116 (2020)
    PLoS Pathogens, Vol 15, Iss 12, p e1008185 (2019)
    PLoS Pathogens

    مصطلحات موضوعية: 0209 industrial biotechnology, viruses, Gene Expression, 02 engineering and technology, Virus Replication, Pathology and Laboratory Medicine, Endoplasmic Reticulum, 01 natural sciences, Biochemistry, Virions, 020901 industrial engineering & automation, Medicine and Health Sciences, Post-Translational Modification, Phosphorylation, Biology (General), ATF6, 0303 health sciences, Secretory Pathway, Messenger RNA, 030302 biochemistry & molecular biology, Herpesviridae Infections, Kaposi's Sarcoma-Associated Herpesvirus, unfolded protein response, Endoplasmic Reticulum Stress, Cell biology, Virus Latency, Nucleic acids, Lytic cycle, Medical Microbiology, Cell Processes, Viral Pathogens, Herpesvirus 8, Human, Viruses, Pathogens, Cellular Structures and Organelles, Research Article, PERK, Herpesviruses, XBP1, QH301-705.5, Immunology, DNA transcription, lcsh:A, KSHV, IRE1, Biology, Viral Structure, Microbiology, Cell Line, 03 medical and health sciences, Virology, DNA-binding proteins, Genetics, Humans, Gene Regulation, Molecular Biology, Transcription factor, Microbial Pathogens, 030304 developmental biology, lytic, 010401 analytical chemistry, ATF4, Organisms, Biology and Life Sciences, Proteins, Cell Biology, biochemical phenomena, metabolism, and nutrition, RC581-607, Viral Replication, 0104 chemical sciences, Regulatory Proteins, Viral replication, Unfolded protein response, RNA, Parasitology, Ectopic expression, Virus Activation, Immunologic diseases. Allergy, lcsh:General Works, DNA viruses, Transcription Factors

    الوصف: Herpesviruses usurp host cell protein synthesis machinery to convert viral mRNAs into proteins, and the endoplasmic reticulum (ER) to ensure proper folding, post-translational modification and trafficking of secreted and transmembrane viral proteins. Overloading ER folding capacity activates the unfolded protein response (UPR), whereby sensor proteins ATF6, PERK and IRE1 initiate a stress-mitigating transcription program that accelerates catabolism of misfolded proteins while increasing ER folding capacity. Kaposi’s sarcoma-associated herpesvirus (KSHV) can be reactivated from latency by chemical induction of ER stress, which causes accumulation of the XBP1s transcription factor that transactivates the viral RTA lytic switch gene. The presence of XBP1s-responsive elements in the RTA promoter suggests that KSHV evolved a mechanism to respond to ER stress. Here, we report that ATF6, PERK and IRE1 were activated upon reactivation from latency and required for efficient KSHV lytic replication; genetic or pharmacologic inhibition of each UPR sensor diminished virion production. Despite UPR sensor activation during KSHV lytic replication, downstream UPR transcriptional responses were restricted; 1) ATF6 was cleaved to activate the ATF6(N) transcription factor but ATF6(N)-responsive genes were not transcribed; 2) PERK phosphorylated eIF2α but ATF4 did not accumulate; 3) IRE1 caused XBP1 mRNA splicing, but XBP1s protein did not accumulate and XBP1s-responsive genes were not transcribed. Ectopic expression of the KSHV host shutoff protein SOX did not affect UPR gene expression, suggesting that alternative viral mechanisms likely mediate UPR suppression during lytic replication. Complementation of XBP1s deficiency during KSHV lytic replication inhibited virion production in a dose-dependent manner in iSLK.219 cells but not in TREx-BCBL1-RTA cells. However, genetically distinct KSHV virions harvested from these two cell lines were equally susceptible to XBP1s restriction following infection of naïve iSLK cells. This suggests that cell-intrinsic properties of BCBL1 cells may circumvent the antiviral effect of ectopic XBP1s expression. Taken together, these findings indicate that while XBP1s plays an important role in reactivation from latency, it can inhibit virus replication at a later step, which the virus overcomes by preventing its synthesis. These findings suggest that KSHV hijacks UPR sensors to promote efficient viral replication while sustaining ER stress.
    Author summary Like all viruses, Kaposi’s sarcoma-associated herpesvirus (KSHV) uses cellular machinery to create viral proteins. Some of these proteins are folded and modified in the endoplasmic reticulum (ER) and traverse the cellular secretory apparatus. Exceeding ER protein folding capacity activates the unfolded protein response (UPR), which resolves ER stress by putting the brakes on protein synthesis and turning on stress-mitigating genes. We show that KSHV replication activates the three cellular proteins that sense ER stress, which are each required to support efficient viral replication. By contrast, KSHV blocks the UPR gene expression program downstream from each of these activated sensor proteins. The failure to resolve ER stress might normally be expected to put the virus at a disadvantage, but we demonstrate that reversal of this scenario is worse; when we supplement infected epithelial cells with the UPR transcription factor XBP1s to artificially stimulate the production of UPR-responsive gene products, virus replication is blocked at a late stage and very few viruses are released from infected cells. Taken together, these observations suggest that KSHV requires UPR sensor protein activation to replicate but has dramatically altered the outcome to prevent the synthesis of new UPR proteins and sustain stress in the ER compartment.

  6. 6

    المؤلفون: Yongchang Cao, Zhichao Xu, Yun Zhang

    المصدر: Viruses, Vol 13, Iss 1698, p 1698 (2021)
    Viruses

    الوصف: Avian infectious bronchitis virus (IBV) is an important gammacoronavirus. The virus is highly contagious, can infect chickens of all ages, and causes considerable economic losses in the poultry industry worldwide. In the last few decades, numerous studies have been published regarding pathogenicity, vaccination, and host immunity-virus interaction. In particular, innate immunity serves as the first line of defense against invasive pathogens and plays an important role in the pathogenetic process of IBV infection. This review focuses on fundamental aspects of host innate immune responses after IBV infection, including identification of conserved viral structures and different components of host with antiviral activity, which could provide useful information for novel vaccine development, vaccination strategies, and intervention programs.

  7. 7

    المؤلفون: Elizabeth R. Wright

    المصدر: Viruses, Vol 2, Iss 1, Pp 107-110 (2010)
    Viruses

    الوصف: Commentary on Byeon, I.J.; Meng, X.; Jung, J.; Zhao, G.; Yang, R.; Ahn, J.; Shi, J.; Concel, J.; Aiken, C.; Zhang, P.; Gronenborn, A.M. Structural convergence between Cryo-EM and NMR reveals intersubunit interactions critical for HIV-1 capsid function. Cell 2009, 139, 780–790.