Introduction to Human Viruses - Daniel N
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New Insights to Adenovirus-Directed Innate Immunity in Respiratory Epithelial Cells
microorganisms Review New Insights to Adenovirus-Directed Innate Immunity in Respiratory Epithelial Cells Cathleen R. Carlin Department of Molecular Biology and Microbiology and the Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA; [email protected]; Tel.: +216-368-8939 Received: 24 June 2019; Accepted: 19 July 2019; Published: 25 July 2019 Abstract: The nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) family of transcription factors is a key component of the host innate immune response to infectious adenoviruses and adenovirus vectors. In this review, we will discuss a regulatory adenoviral protein encoded by early region 3 (E3) called E3-RIDα, which targets NFκB through subversion of novel host cell pathways. E3-RIDα down-regulates an EGF receptor signaling pathway, which overrides NFκB negative feedback control in the nucleus, and is induced by cell stress associated with viral infection and exposure to the pro-inflammatory cytokine TNF-α. E3-RIDα also modulates NFκB signaling downstream of the lipopolysaccharide receptor, Toll-like receptor 4, through formation of membrane contact sites controlling cholesterol levels in endosomes. These innate immune evasion tactics have yielded unique perspectives regarding the potential physiological functions of host cell pathways with important roles in infectious disease. Keywords: adenovirus; early region 3; innate immunity; NFκB 1. Introduction Adenoviruses have proven to be invaluable experimental tools contributing to many breakthrough discoveries, including mRNA splicing and antigen presentation to T cells [1,2]. The finding that adenovirus type 12 caused cancer in hamsters in a laboratory setting was the first example of oncogenic activity by a human virus [3]. -
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. -
Apoptosis in Viral Pathogenesis
Cell Death and Differentiation (2001) 8, 109 ± 110 ã 2001 Nature Publishing Group All rights reserved 1350-9047/01 $15.00 www.nature.com/cdd Editorial Apoptosis in viral pathogenesis JM Hardwick*,1,2,3,4,5 with an unusual deg (degradation) phenotype,1,2 leading to an understanding of how E1b 55K and E1b 19K inhibit apoptotic 1 Department of Molecular Microbiology and Immunology, Johns Hopkins cell death by distinct mechanisms. Lois Miller's laboratory University Schools of Public Health and Medicine, Baltimore, Maryland 21205, made a link to virus-induced disease when they demonstrated USA that the baculovirus-encoded caspase inhibitor P35 was 2 Department of Neurology, Johns Hopkins University Schools of Public Health required for pathogenesis.3,4 Jeurissen et al. first associated and Medicine, Baltimore, Maryland 21205, USA 3 Department of Pharmacology and Molecular Sciences, Johns Hopkins virus-induced apoptosis with disease in chickens when they University Schools of Public Health and Medicine, Baltimore, Maryland 21205, showed that chicken anemia virus infection of hatchlings USA resulted in thymocyte apoptosis.5 Cellular anti-apoptotic 4 Department of Biochemistry and Molecular Biology, Johns Hopkins University genes were then found to convert a lytic virus infection to a Schools of Public Health and Medicine, Baltimore, Maryland 21205, USA persistent infection, perhaps explaining the long-term 5 Department of Oncology, Johns Hopkins University Schools of Public Health persistence of alphaviruses in the brain.6 Early in the and Medicine, Baltimore, Maryland 21205, USA * Corresponding author: JM Hardwick, Department of Molecular Microbiology apoptosis field, a number of laboratories gathered evidence 7 and Immunology, Johns Hopkins University Schools of Public Health and for HIV-triggered apoptosis in AIDS. -
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. -
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. -
Viruses of Respiratory Tract: an Observational Retrospective Study on Hospitalized Patients in Rome, Italy
microorganisms Article Viruses of Respiratory Tract: an Observational Retrospective Study on Hospitalized Patients in Rome, Italy 1, 2, 2 3 3 Marco Ciotti y , Massimo Maurici y, Viviana Santoro , Luigi Coppola , Loredana Sarmati , Gerardo De Carolis 4, Patrizia De Filippis 2 and Francesca Pica 5,* 1 Unit of Virology Fondazione Policlinico Tor Vergata, 00133 Rome, Italy; [email protected] 2 Department of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy; [email protected] (M.M.); [email protected] (V.S.); patrizia.de.fi[email protected] (P.D.F.) 3 Clinical Infectious Diseases, Fondazione Policlinico Tor Vergata, 00133 Rome, Italy; [email protected] (L.C.); [email protected] (L.S.) 4 Health Management, Fondazione Policlinico Tor Vergata, 00133 Rome, Italy; [email protected] 5 Department of Experimental Medicine, University of Rome Tor Vergata, 00133 Rome, Italy * Correspondence: [email protected]; Tel.:+39-6-72596462/39-6-72596184 These authors contributed equally to this work. y Received: 4 March 2020; Accepted: 30 March 2020; Published: 1 April 2020 Abstract: Respiratory tract infections account for high morbidity and mortality around the world. Fragile patients are at high risk of developing complications such as pneumonia and may die from it. Limited information is available on the extent of the circulation of respiratory viruses in the hospital setting. Most knowledge relates to influenza viruses (FLU) but several other viruses produce flu-like illness. The study was conducted at the University Hospital Policlinico Tor Vergata, Rome, Italy. Clinical and laboratory data from hospitalized patients with respiratory tract infections during the period October 2016–March 2019 were analysed. -
Viral Pathogenesis: Influenza Knows How to Exploit Its Host
RESEARCH HIGHLIGHTS IN BRIEF BACTERIAL PATHOGENESIS More to CRISPR than adaptive immunity A new study shows that the type II CRISPR–Cas (clustered, regularly interspaced short palindromic repeats– CRISPR-associated proteins) system of the intracellular pathogen Francisella novicida downregulates the expression of an immunostimulatory bacterial lipoprotein (BLP), which increases the integrity of the cell envelope, resulting in antibiotic resistance and inflammasome evasion. Sampson et al. found that a mutant that lacked the endonuclease Cas9 was resistant to the membrane-targeting antibiotic polymyxin B, and in combination with its partner RNAs (the tracrRNA and scaRNA), Cas9 directly enhanced envelope integrity in vitro and during intracellular infection, owing, at least in part, to reduced expression of BLP. Furthermore, evasion of the AIM2– ASC inflammasome (which is activated by Toll-like receptor 2 (TLR2)) was Cas9‑dependent, and the reduced virulence of the cas9-null mutant was restored in the absence of both ASC and TLR2, which demonstrates the pivotal role of Cas9 in evading innate immunity. Further to its role in adaptive immunity, this study shows that CRISPR–Cas is an important determinant of gene expression and contributes to bacterial pathogenesis. ORIGINAL RESEARCH PAPER Sampson, T. R. et al. A CRISPR–Cas system enhances envelope integrity mediating antibiotic resistance and inflammasome evasion. Proc. Natl Acad. Sci. USA 111, 11163–11168 (2014) VIRAL PATHOGENESIS Influenza knows how to exploit its host During budding from the plasma membrane, influenza A viruses (IAVs) incorporate host proteins, but the role of these proteins in the viral life cycle is poorly understood. Berri et al. now show that the membrane protein annexin V (A5), which is upregulated during IAV infection and is incorporated into viral particles, enables escape from immune detection. -
Update on Viral Pathogenesis in BRD
*c Cambridge University Press 2009 Animal Health Research Reviews 10(2); 149–153 ISSN 1466-2523 doi:10.1017/S146625230999020X Update on viral pathogenesis in BRD John A. Ellis Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK S7N 5B4, Canada Received 12 August 2009; Accepted 18 October 2009 Abstract Many viruses, including bovine herpesvirus-1 (BHV-1), bovine respiratory syncytial virus (BRSV), parainfluenzavirus-3 (PI3), bovine coronavirus, bovine viral diarrhea virus and bovine reovirus, have been etiologically associated with respiratory disease in cattle. This review focuses on the pathogenesis of BHV-1 and BRSV, two very different agents that primarily cause disease in the upper and lower respiratory tract, respectively. Keywords: bovine herpesvirus-1, bovine respiratory syncytial virus, immune response, immunosuppression, bovine respiratory, bovine herpesvirus, latency-related (LR), bovine respiratory disease, open reading frame (ORF-E) Bovine herpesvirus-1 (BHV-1): what are its and Chowdhury, 2008). Mechanisms of maintenance of characteristics? latency are not completely understood, but are associated with high levels of transcription of latency-related (LR) First isolated in 1956 (Madin et al., 1956), BHV-1 is a and open reading frame (ORF-E) genes. Conversely, representative of the Alphaherpesvirinae, which as a recrudesence/reactivation of latent BHV-1 and resultant group, cause similar upper respiratory tract diseases in replication in epithelia of the upper respiratory tract are a wide range of host species. These viruses are large associated with reduced expression of LR and ORF-E (135 kB), double-stranded DNA viruses composed of genes together with increased expression of other viral an icosahedral nucleocapsid, and envelope that are genes (Muylkens et al., 2007; Jones and Chowdhury, connected by a ‘tegment’. -
1 Chapter I Overall Issues of Virus and Host Evolution
CHAPTER I OVERALL ISSUES OF VIRUS AND HOST EVOLUTION tree of life. Yet viruses do have the This book seeks to present the evolution of characteristics of life, can be killed, can become viruses from the perspective of the evolution extinct and adhere to the rules of evolutionary of their host. Since viruses essentially infect biology and Darwinian selection. In addition, all life forms, the book will broadly cover all viruses have enormous impact on the evolution life. Such an organization of the virus of their host. Viruses are ancient life forms, their literature will thus differ considerably from numbers are vast and their role in the fabric of the usual pattern of presenting viruses life is fundamental and unending. They according to either the virus type or the type represent the leading edge of evolution of all of host disease they are associated with. In living entities and they must no longer be left out so doing, it presents the broad patterns of the of the tree of life. evolution of life and evaluates the role of viruses in host evolution as well as the role Definitions. The concept of a virus has old of host in virus evolution. This book also origins, yet our modern understanding or seeks to broadly consider and present the definition of a virus is relatively recent and role of persistent viruses in evolution. directly associated with our unraveling the nature Although we have come to realize that viral of genes and nucleic acids in biological systems. persistence is indeed a common relationship As it will be important to avoid the perpetuation between virus and host, it is usually of some of the vague and sometimes inaccurate considered as a variation of a host infection views of viruses, below we present some pattern and not the basis from which to definitions that apply to modern virology. -
The Inequality Virus Bringing Together a World Torn Apart by Coronavirus Through a Fair, Just and Sustainable Economy
Adam Dicko is a Malian activist, fighting for social justice in the times of COVID-19 © Xavier Thera/Oxfam The Inequality Virus Bringing together a world torn apart by coronavirus through a fair, just and sustainable economy www.oxfam.org OXFAM BRIEFING PAPER – JANUARY 2021 The coronavirus pandemic has the potential to lead to an increase in inequality in almost every country at once, the first time this has happened since records began. The virus has exposed, fed off and increased existing inequalities of wealth, gender and race. Over two million people have died, and hundreds of millions of people are being forced into poverty while many of the richest – individuals and corporations – are thriving. Billionaire fortunes returned to their pre-pandemic highs in just nine months, while recovery for the world’s poorest people could take over a decade. The crisis has exposed our collective frailty and the inability of our deeply unequal economy to work for all. Yet it has also shown us the vital importance of government action to protect our health and livelihoods. Transformative policies that seemed unthinkable before the crisis have suddenly been shown to be possible. There can be no return to where we were before. Instead, citizens and governments must act on the urgency to create a more equal and sustainable world. 2 © Oxfam International January 2021 This paper was written by Esmé Berkhout, Nick Galasso, Max Lawson, Pablo Andrés Rivero Morales, Anjela Taneja, and Diego Alejo Vázquez Pimentel. Oxfam acknowledges the assistance of Jaime