Conceptualizing the Virus by Suzanne Banas
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Multiple Origins of Viral Capsid Proteins from Cellular Ancestors
Multiple origins of viral capsid proteins from PNAS PLUS cellular ancestors Mart Krupovica,1 and Eugene V. Kooninb,1 aInstitut Pasteur, Department of Microbiology, Unité Biologie Moléculaire du Gène chez les Extrêmophiles, 75015 Paris, France; and bNational Center for Biotechnology Information, National Library of Medicine, Bethesda, MD 20894 Contributed by Eugene V. Koonin, February 3, 2017 (sent for review December 21, 2016; reviewed by C. Martin Lawrence and Kenneth Stedman) Viruses are the most abundant biological entities on earth and show genome replication. Understanding the origin of any virus group is remarkable diversity of genome sequences, replication and expres- possible only if the provenances of both components are elucidated sion strategies, and virion structures. Evolutionary genomics of (11). Given that viral replication proteins often have no closely viruses revealed many unexpected connections but the general related homologs in known cellular organisms (6, 12), it has been scenario(s) for the evolution of the virosphere remains a matter of suggested that many of these proteins evolved in the precellular intense debate among proponents of the cellular regression, escaped world (4, 6) or in primordial, now extinct, cellular lineages (5, 10, genes, and primordial virus world hypotheses. A comprehensive 13). The ability to transfer the genetic information encased within sequence and structure analysis of major virion proteins indicates capsids—the protective proteinaceous shells that comprise the that they evolved on about 20 independent occasions, and in some of cores of virus particles (virions)—is unique to bona fide viruses and these cases likely ancestors are identifiable among the proteins of distinguishes them from other types of selfish genetic elements cellular organisms. -
Imaging, Tracking and Computational Analyses of Virus Entry and Egress
1 Review 2 Imaging, Tracking and Computational Analyses of 3 Virus Entry and Egress with the Cytoskeleton 4 I-Hsuan Wang 1,†, Christoph J. Burckhardt 2,†, A. Yakimovich 3 and Urs F. Greber 4,* 5 1 Division of Virology, Institute of Medical Science, tHe University of ToKyo, ToKyo 108-8639, Japan 6 2 UT SoutHwestern Medical Center, Lyda Hill Department of Bioinformatics, Dallas TX 75390, USA 7 3 MRC Laboratory for Molecular Cell Biology, University College London, London, United Kingdom 8 4 Department of Molecular Life Sciences, University of ZuricH, WintertHurerstrasse 190, CH-8057 ZuricH, 9 Switzerland 10 * Correspondence: [email protected], Telephone: +41 44 635 4841, Fax: +41 44 635 6817 11 † These autHors contributed equally to tHis work. 12 Received: date; Accepted: date; PublisHed: date 13 Abstract: Viruses Have a dual nature - particles are ‘passive substances’ lacKing chemical energy 14 transformation, wHereas infected cells are ‘active substances’ turning-over energy. How passive 15 viral substances convert to active substances, comprising viral replication and assembly 16 compartments Has been of intense interest to virologists, cell and molecular biologists and 17 immunologists. Infection starts witH virus entry into a susceptible cell and delivers tHe viral 18 genome to the replication site. THis is a multi-step process, and involves tHe cytosKeleton and 19 associated motor proteins. LiKewise, the egress of progeny virus particles from the replication site 20 to the extracellular space is enHanced by tHe cytosKeleton and associated motor proteins. THis 21 overcomes tHe limitation of tHermal diffusion, and transports virions and virion components, 22 often in association witH cellular organelles. -
An Expanded View of Viruses
An Expanded View of Viruses Urs F. Greber 1) & Ralf Bartenschlager 2) 1) Department of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland 2) Department of Infectious Diseases, Molecular Virology, Heidelberg University, Im Neuenheimer Feld 345, 69198 Heidelberg, Germany Correspondence to: [email protected] [email protected] 1 figure Keywords: Zoonosis; Pandemics; Dengue, Ebola; Influenza; Entry; Endocytosis; Uncoating; Transport; Filovirus; Comparative genomics; Computational analyses; Virus-host interactions; Filamentous virus; Bacterial biofilm; Phage; Bacteriophage; Glycan; Immunity; Infection; Disease; Evolution; Variability; Giant virus; Ferret; Guinea pig; Emerging disease; Pandemic; Host range; Enveloped virus; 1 Viruses are ubiquitous, and are important in medicine, biology, biotechnology and ecology. All kinds of cells can be infected with viruses, and sometimes, a particular cell is infected with different viruses at the same time. The virus particle, ‘virion’ is composed of the viral coat proteins sheltering the viral genome, and is often surrounded by a lipid “envelope”. A virion is small compared to cells, and when it enters cells gives rise to infection distinct from an intracellular bacterial pathogen (Lwoff, 1957). A virus-infected cell has a profoundly altered homeostasis due to numerous interactions between cellular and viral components. This leads to evolutionary pressure on both virus and host, and argues that viruses are a part of life (Ludmir & Enquist, 2009). Our cells can be infected by viruses causing acute disease, such as respiratory disease by Influenza virus or rhinoviruses, or chronic disease, such as hepatitis or immune deficiency. However, most viral attacks on cells are fend off, or the spread of viruses in an infected organism is restricted, and infection abrogated. -
An Introduction to the Viruses
Chapter 1 An introduction to the viruses Viruses are obligate intracellular parasites of man, other animals, plants and bacteria. They can only multiply within cells, and thus differ from bacteria, which can multiply in tissues in an extracellular position, and also in artificial culture media in the laboratory. It has always been recognized that viruses are distinct from the bacteria, but originally other groups of infective agents were included among the viruses which are now known to be organisms of a different and more complex nature. These included the Chlamydiae, organisms causing diseases such as lymphogranuloma venereum and trachoma, and the Rickettsiae, the causative agents of typhus and related infections. The specific treatment of infections caused by these two groups of agents will not be considered in this work, which is restricted to the chemotherapy of infections caused by the true viruses. The Chlamydiae and Rickettsiae are complete organisms, with cell walls, which possess both types of nucleic acid, enzyme systems which function within their cytoplasm, and a number of cell organelles. The viruses, on the other hand, possess either DNA or RNA as their genetic material, but not both. In some cases they contain enzymes, but these exert their functions within the host cell after the virus particle has under gone a process of dissolution during the early stage of infection. Except in the case of the arenaviruses, a group which contains the virus of Lassa fever, the virus particles do not contain organelles. A virus is thus much more rudimentary in structure, and relies upon the host cell to provide the systems for synthesizing its components which it does not possess itself. -
Theory of an Immune System Retrovirus
Proc. Nati. Acad. Sci. USA Vol. 83, pp. 9159-9163, December 1986 Medical Sciences Theory of an immune system retrovirus (human immunodeficiency virus/acquired immune deficiency syndrome) LEON N COOPER Physics Department and Center for Neural Science, Brown University, Providence, RI 02912 Contributed by Leon N Cooper, July 23, 1986 ABSTRACT Human immunodeficiency virus (HIV; for- initiates clonal expansion, sustained by interleukin 2 and y merly known as human T-cell lymphotropic virus type interferon. Ill/lymphadenopathy-associated virus, HTLV-Ill/LAV), the I first give a brief sketch of these events in a linked- retrovirus that infects T4-positive (helper) T cells of the interaction model in which it is assumed that antigen-specific immune system, has been implicated as the agent responsible T cells must interact with the B-cell-processed virus to for the acquired immune deficiency syndrome. In this paper, initiate clonal expansion (2). I then assume that virus-specific I contrast the growth of a "normal" virus with what I call an antibody is the major component ofimmune system response immune system retrovirus: a retrovirus that attacks the T4- that limits virus spread. As will be seen, the details of these positive T cells of the immune system. I show that remarkable assumptions do not affect the qualitative features of my interactions with other infections as well as strong virus conclusions. concentration dependence are general properties of immune Linked-Interaction Model for Clonal Expansion of Lympho- system retroviruses. Some of the consequences of these ideas cytes. Let X be the concentration of normal infecting virus are compared with observations. -
How Influenza Virus Uses Host Cell Pathways During Uncoating
cells Review How Influenza Virus Uses Host Cell Pathways during Uncoating Etori Aguiar Moreira 1 , Yohei Yamauchi 2 and Patrick Matthias 1,3,* 1 Friedrich Miescher Institute for Biomedical Research, 4058 Basel, Switzerland; [email protected] 2 Faculty of Life Sciences, School of Cellular and Molecular Medicine, University of Bristol, Bristol BS8 1TD, UK; [email protected] 3 Faculty of Sciences, University of Basel, 4031 Basel, Switzerland * Correspondence: [email protected] Abstract: Influenza is a zoonotic respiratory disease of major public health interest due to its pan- demic potential, and a threat to animals and the human population. The influenza A virus genome consists of eight single-stranded RNA segments sequestered within a protein capsid and a lipid bilayer envelope. During host cell entry, cellular cues contribute to viral conformational changes that promote critical events such as fusion with late endosomes, capsid uncoating and viral genome release into the cytosol. In this focused review, we concisely describe the virus infection cycle and highlight the recent findings of host cell pathways and cytosolic proteins that assist influenza uncoating during host cell entry. Keywords: influenza; capsid uncoating; HDAC6; ubiquitin; EPS8; TNPO1; pandemic; M1; virus– host interaction Citation: Moreira, E.A.; Yamauchi, Y.; Matthias, P. How Influenza Virus Uses Host Cell Pathways during 1. Introduction Uncoating. Cells 2021, 10, 1722. Viruses are microscopic parasites that, unable to self-replicate, subvert a host cell https://doi.org/10.3390/ for their replication and propagation. Despite their apparent simplicity, they can cause cells10071722 severe diseases and even pose pandemic threats [1–3]. -
Persistent Virus and Addiction Modules: an Engine of Symbiosis
UC Irvine UC Irvine Previously Published Works Title Persistent virus and addiction modules: an engine of symbiosis. Permalink https://escholarship.org/uc/item/5ck1g026 Journal Current opinion in microbiology, 31 ISSN 1369-5274 Author Villarreal, Luis P Publication Date 2016-06-01 DOI 10.1016/j.mib.2016.03.005 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Available online at www.sciencedirect.com ScienceDirect Persistent virus and addiction modules: an engine of symbiosis Luis P Villarreal The giant DNA viruses are highly prevalent and have a particular host would occasionally survive but still retain a bit of affinity for the lytic infection of unicellular eukaryotic host. The the selfish virus DNA. Thus although parasitic selfish giant viruses can also be infected by inhibitory virophage which (virus-like) information is common in the genomes of all can provide lysis protection to their host. The combined life forms, its presence was explained as mostly defective protective and destructive action of such viruses can define a remnants of past plague sweeps that provides no func- general model (PD) of virus-mediated host survival. Here, I tional benefit to the host (e.g. junk). Until recently, this present a general model for role such viruses play in the explanation seemed satisfactory. In the last twenty years, evolution of host symbiosis. By considering how virus mixtures however, various observation-based developments have can participate in addiction modules, I provide a functional compelled us to re-evaluate this stance. Both comparative explanation for persistence of virus derived genetic ‘junk’ in genomics and metagenomics (sequencing habitats) has their host genomic habitats. -
West Nile Virus (WNV) Fact Sheet
West Nile Virus (WNV) Fact Sheet What Is West Nile Virus? How Does West Nile Virus Spread? West Nile virus infection can cause serious disease. WNV is ▪ Infected Mosquitoes. established as a seasonal epidemic in North America that WNV is spread by the bite of an infected mosquito. flares up in the summer and continues into the fall. This Mosquitoes become infected when they feed on fact sheet contains important information that can help infected birds. Infected mosquitoes can then spread you recognize and prevent West Nile virus. WNV to humans and other animals when they bite. What Can I Do to Prevent WNV? ▪ Transfusions, Transplants, and Mother-to-Child. In a very small number of cases, WNV also has been The easiest and best way to avoid WNV is to prevent spread directly from an infected person through blood mosquito bites. transfusions, organ transplants, breastfeeding and ▪ When outdoors, use repellents containing DEET, during pregnancy from mother to baby. picaridin, IR3535, some oil of lemon eucalyptus or para- Not through touching. menthane-diol. Follow the directions on the package. ▪ WNV is not spread through casual contact such as ▪ Many mosquitoes are most active from dusk to dawn. touching or kissing a person with the virus. Be sure to use insect repellent and wear long sleeves and pants at these times or consider staying indoors How Soon Do Infected People Get Sick? during these hours. People typically develop symptoms between 3 and 14 days after they are bitten by the infected mosquito. ▪ Make sure you have good screens on your windows and doors to keep mosquitoes out. -
Constructing Protocells: a Second Origin of Life
04_SteenRASMUSSEN.qxd:Maqueta.qxd 4/6/12 11:45 Página 585 Session I: The Physical Mind CONSTRUCTING PROTOCELLS: A SECOND ORIGIN OF LIFE STEEN RASMUSSEN Center for Fundamental Living Technology (FLinT) Santa Fe Institute, New Mexico USA ANDERS ALBERTSEN, PERNILLE LYKKE PEDERSEN, CARSTEN SVANEBORG Center for Fundamental Living Technology (FLinT) ABSTRACT: What is life? How does nonliving materials become alive? How did the first living cells emerge on Earth? How can artificial living processes be useful for technology? These are the kinds of questions we seek to address by assembling minimal living systems from scratch. INTRODUCTION To create living materials from nonliving materials, we first need to understand what life is. Today life is believed to be a physical process, where the properties of life emerge from the dynamics of material interactions. This has not always been the assumption, as living matter at least since the origin of Hindu medicine some 5000 years ago, was believed to have a metaphysical vital force. Von Neumann, the inventor of the modern computer, realized that if life is a physical process it should be possible to implement life in other media than biochemistry. In the 1950s, he was one of the first to propose the possibilities of implementing living processes in computers and robots. This perspective, while being controversial, is gaining momentum in many scientific communities. There is not a generally agreed upon definition of life within the scientific community, as there is a grey zone of interesting processes between nonliving and living matter. Our work on assembling minimal physicochemical life is based on three criteria, which most biological life forms satisfy. -
Virus World As an Evolutionary Network of Viruses and Capsidless Selfish Elements
Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements Koonin, E. V., & Dolja, V. V. (2014). Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements. Microbiology and Molecular Biology Reviews, 78(2), 278-303. doi:10.1128/MMBR.00049-13 10.1128/MMBR.00049-13 American Society for Microbiology Version of Record http://cdss.library.oregonstate.edu/sa-termsofuse Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements Eugene V. Koonin,a Valerian V. Doljab National Center for Biotechnology Information, National Library of Medicine, Bethesda, Maryland, USAa; Department of Botany and Plant Pathology and Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon, USAb Downloaded from SUMMARY ..................................................................................................................................................278 INTRODUCTION ............................................................................................................................................278 PREVALENCE OF REPLICATION SYSTEM COMPONENTS COMPARED TO CAPSID PROTEINS AMONG VIRUS HALLMARK GENES.......................279 CLASSIFICATION OF VIRUSES BY REPLICATION-EXPRESSION STRATEGY: TYPICAL VIRUSES AND CAPSIDLESS FORMS ................................279 EVOLUTIONARY RELATIONSHIPS BETWEEN VIRUSES AND CAPSIDLESS VIRUS-LIKE GENETIC ELEMENTS ..............................................280 Capsidless Derivatives of Positive-Strand RNA Viruses....................................................................................................280 -
Capsid Structures, Variation and Flexibility. This Project Brings Together the Skills of Laboratories at Cornell University
Principal Investigator/Program Director (Last, first, middle): Parrish, Colin, R. Capsid structures, variation and flexibility. This project brings together the skills of laboratories at Cornell University and at Pennsylvania State University Medical Center to provide a detailed understanding of the roles of structural variation and flexibility in the parvoviral capsid, and their effects on receptor and antibody binding and the controls of cell infection and host range. These are fundamental problems that apply to all animal viruses, where the capsid must protect the genome in the environment, interact with host molecules including cell receptors and antibodies, and undergo a series of regulated structural transitions during cell entry to eventually release the genome for replication. Viral capsid binding to host receptors and antibodies can have varying and often unpredictable effects on infection, and those interactions also control many other replication steps. Where these virus-host interactions are specific they can control the viral host ranges. A model for understanding virus cell infection and host range control through differential receptor binding. We study two viruses that differ in host range due to 3 or 4 capsid protein mutations that control specific receptor binding. Canine parvovirus (CPV) arose around 1976 as a variant of feline panleukopenia virus (FPV), and caused a pandemic of disease during 1978 and 1979. That virus has continued to circulate worldwide as a serious canine pathogen, and has also evolved new antigenic, receptor binding, and host range variants. FPV and CPV both can bind the feline transferrin receptor 1 (TfR) to infect cat cells, and CPV gained the host range for dogs by gaining the ability to bind the canine TfR. -
Viral Infection Modulates Mitochondrial Function
International Journal of Molecular Sciences Review Viral Infection Modulates Mitochondrial Function Xiaowen Li 1,2,3, Keke Wu 1,2,3, Sen Zeng 1,2,3, Feifan Zhao 1,2,3, Jindai Fan 1,2,3, Zhaoyao Li 1,2,3, Lin Yi 1,2,3, Hongxing Ding 1,2,3, Mingqiu Zhao 1,2,3, Shuangqi Fan 1,2,3,* and Jinding Chen 1,2,3,* 1 College of Veterinary Medicine, South China Agricultural University, No. 483 Wushan Road, Tianhe District, Guangzhou 510642, China; [email protected] (X.L.); [email protected] (K.W.); [email protected] (S.Z.); [email protected] (F.Z.); [email protected] (J.F.); [email protected] (Z.L.); [email protected] (L.Y.); [email protected] (H.D.); [email protected] (M.Z.) 2 Guangdong Laboratory for Lingnan Modern Agriculture, College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China 3 Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, Guangzhou 510642, China * Correspondence: [email protected] (S.F.); [email protected] (J.C.); Tel.: +86-20-8528-8017 (S.F.); +86-20-8528-8017 (J.C.) Abstract: Mitochondria are important organelles involved in metabolism and programmed cell death in eukaryotic cells. In addition, mitochondria are also closely related to the innate immunity of host cells against viruses. The abnormality of mitochondrial morphology and function might lead to a variety of diseases. A large number of studies have found that a variety of viral infec- tions could change mitochondrial dynamics, mediate mitochondria-induced cell death, and alter the mitochondrial metabolic status and cellular innate immune response to maintain intracellular survival.