The History of Vaccines Lesson Plan: Viruses and Evolution
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Mutational Load Causes Stochastic Evolutionary Outcomes In
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Apollo Virus Evolution, 2019, 5(1): vez008 doi: 10.1093/ve/vez008 Research article Mutational load causes stochastic evolutionary outcomes in acute RNA viral infection Downloaded from https://academic.oup.com/ve/article-abstract/5/1/vez008/5476199 by guest on 01 June 2020 Lei Zhao,1,† Ali B. Abbasi,1 and Christopher J. R. Illingworth1,2,*,‡ 1Department of Genetics, University of Cambridge, Cambridge, UK and 2Department of Applied Mathematics and Theoretical Physics, University of Cambridge, Cambridge, UK *Corresponding author: E-mail: [email protected] †http://orcid.org/0000-0002-6551-2707 ‡http://orcid.org/0000-0002-0030-2784 Abstract Mutational load is known to be of importance for the evolution of RNA viruses, the combination of a high mutation rate and large population size leading to an accumulation of deleterious mutations. However, while the effects of mutational load on global viral populations have been considered, its quantitative effects at the within-host scale of infection are less well un- derstood. We here show that even on the rapid timescale of acute disease, mutational load has an effect on within-host vi- ral adaptation, reducing the effective selection acting upon beneficial variants by 10 per cent. Furthermore, mutational load induces considerable stochasticity in the pattern of evolution, causing a more than five-fold uncertainty in the effective fitness of a transmitted beneficial variant. Our work aims to bridge the gap between classic models from population genetic theory and the biology of viral infection. -
Changes in Population Dynamics in Mutualistic Versus Pathogenic Viruses
Viruses 2011, 3, 12-19; doi:10.3390/v3010012 OPEN ACCESS viruses ISSN 1999-4915 www.mdpi.com/journal/viruses Commentary Changes in Population Dynamics in Mutualistic versus Pathogenic Viruses Marilyn J. Roossinck Plant Biology Division, The Samuel Roberts Noble Foundation, Inc., P.O. Box 2180, Ardmore, OK 73402, USA; E-Mail: [email protected]; Tel.: +1 580 224 6600; Fax: +1 580 224 6692. Received: 17 December 2010; in revised form: 31 December 2010 / Accepted: 6 January 2011 / Published: 17 January 2011 Abstract: Although generally regarded as pathogens, viruses can also be mutualists. A number of examples of extreme mutualism (i.e., symbiogenesis) have been well studied. Other examples of mutualism are less common, but this is likely because viruses have rarely been thought of as having any beneficial effects on their hosts. The effect of mutualism on the population dynamics of viruses is a topic that has not been addressed experimentally. However, the potential for understanding mutualism and how a virus might become a mutualist may be elucidated by understanding these dynamics. Keywords: beneficial viruses; polymerase fidelity; quasispecies; symbiosis; symbiogenesis 1. Introduction Viruses have been studied predominantly as pathogens, beginning with the first virus ever described, Tobacco mosaic virus [1] that was causing spots on tobacco plants. However, a number of viruses in plants, animals, fungi and bacteria have been described that are not pathogens; many are commensals and some are mutualists. Traditionally, mutualistic symbioses are thought of as long-term stable relationships, but viruses can clearly switch lifestyles depending on conditions. What effect does mutualism have on the population dynamics of a virus? Do the population dynamics of conditional mutualists change depending on their lifestyle? This is the subject of this brief perspective. -
Genetic Engineering and Sustainable Crop Disease Management: Opportunities for Case-By-Case Decision-Making
sustainability Review Genetic Engineering and Sustainable Crop Disease Management: Opportunities for Case-by-Case Decision-Making Paul Vincelli Department of Plant Pathology, 207 Plant Science Building, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40546, USA; [email protected] Academic Editor: Sean Clark Received: 22 March 2016; Accepted: 13 May 2016; Published: 20 May 2016 Abstract: Genetic engineering (GE) offers an expanding array of strategies for enhancing disease resistance of crop plants in sustainable ways, including the potential for reduced pesticide usage. Certain GE applications involve transgenesis, in some cases creating a metabolic pathway novel to the GE crop. In other cases, only cisgenessis is employed. In yet other cases, engineered genetic changes can be so minimal as to be indistinguishable from natural mutations. Thus, GE crops vary substantially and should be evaluated for risks, benefits, and social considerations on a case-by-case basis. Deployment of GE traits should be with an eye towards long-term sustainability; several options are discussed. Selected risks and concerns of GE are also considered, along with genome editing, a technology that greatly expands the capacity of molecular biologists to make more precise and targeted genetic edits. While GE is merely a suite of tools to supplement other breeding techniques, if wisely used, certain GE tools and applications can contribute to sustainability goals. Keywords: biotechnology; GMO (genetically modified organism) 1. Introduction and Background Disease management practices can contribute to sustainability by protecting crop yields, maintaining and improving profitability for crop producers, reducing losses along the distribution chain, and reducing the negative environmental impacts of diseases and their management. -
Zoonotic Diseases Fact Sheet
ZOONOTIC DISEASES FACT SHEET s e ion ecie s n t n p is ms n e e s tio s g s m to a a o u t Rang s p t tme to e th n s n m c a s a ra y a re ho Di P Ge Ho T S Incub F T P Brucella (B. Infected animals Skin or mucous membrane High and protracted (extended) fever. 1-15 weeks Most commonly Antibiotic melitensis, B. (swine, cattle, goats, contact with infected Infection affects bone, heart, reported U.S. combination: abortus, B. suis, B. sheep, dogs) animals, their blood, tissue, gallbladder, kidney, spleen, and laboratory-associated streptomycina, Brucellosis* Bacteria canis ) and other body fluids causes highly disseminated lesions bacterial infection in tetracycline, and and abscess man sulfonamides Salmonella (S. Domestic (dogs, cats, Direct contact as well as Mild gastroenteritiis (diarrhea) to high 6 hours to 3 Fatality rate of 5-10% Antibiotic cholera-suis, S. monkeys, rodents, indirect consumption fever, severe headache, and spleen days combination: enteriditis, S. labor-atory rodents, (eggs, food vehicles using enlargement. May lead to focal chloramphenicol, typhymurium, S. rep-tiles [especially eggs, etc.). Human to infection in any organ or tissue of the neomycin, ampicillin Salmonellosis Bacteria typhi) turtles], chickens and human transmission also body) fish) and herd animals possible (cattle, chickens, pigs) All Shigella species Captive non-human Oral-fecal route Ranges from asymptomatic carrier to Varies by Highly infective. Low Intravenous fluids primates severe bacillary dysentery with high species. 16 number of organisms and electrolytes, fevers, weakness, severe abdominal hours to 7 capable of causing Antibiotics: ampicillin, cramps, prostration, edema of the days. -
Evolutionary Analysis of the Dynamics of Viral Infectious Disease
REVIEWS MODELLING Evolutionary analysis of the dynamics of viral infectious disease Oliver G. Pybus* and Andrew Rambaut‡ Abstract | Many organisms that cause infectious diseases, particularly RNA viruses, mutate so rapidly that their evolutionary and ecological behaviours are inextricably linked. Consequently, aspects of the transmission and epidemiology of these pathogens are imprinted on the genetic diversity of their genomes. Large-scale empirical analyses of the evolutionary dynamics of important pathogens are now feasible owing to the increasing availability of pathogen sequence data and the development of new computational and statistical methods of analysis. In this Review, we outline the questions that can be answered using viral evolutionary analysis across a wide range of biological scales. REFS 5–7 Balancing selection Rapidly evolving pathogens are unique in that their key human pathogens (for example, ). Any form of natural selection ecological and evolutionary dynamics occur on the Understandably, most studies have focused on impor- that results in the maintenance same timescale and can therefore potentially interact. tant human RNA viruses such as influenza virus, HIV, of genetic polymorphisms in a For example, the exceptionally high nucleotide mutation dengue virus and hepatitis C virus (HCV); therefore, this population, as opposed to 1 their loss through fixation or rate of a typical RNA virus — a million times greater Review concentrates on these infections. However, the elimination. than that of vertebrates — allows these viruses to gener- range of pathogens and hosts to which phylodynamic ate mutations and adaptations de novo during environ- methods are applied is expanding, and we also discuss mental change, whereas other organisms must rely on infectious diseases of wildlife, crops and livestock. -
Chapter 2 Disease and Disease Transmission
DISEASE AND DISEASE TRANSMISSION Chapter 2 Disease and disease transmission An enormous variety of organisms exist, including some which can survive and even develop in the body of people or animals. If the organism can cause infection, it is an infectious agent. In this manual infectious agents which cause infection and illness are called pathogens. Diseases caused by pathogens, or the toxins they produce, are communicable or infectious diseases (45). In this manual these will be called disease and infection. This chapter presents the transmission cycle of disease with its different elements, and categorises the different infections related to WES. 2.1 Introduction to the transmission cycle of disease To be able to persist or live on, pathogens must be able to leave an infected host, survive transmission in the environment, enter a susceptible person or animal, and develop and/or multiply in the newly infected host. The transmission of pathogens from current to future host follows a repeating cycle. This cycle can be simple, with a direct transmission from current to future host, or complex, where transmission occurs through (multiple) intermediate hosts or vectors. This cycle is called the transmission cycle of disease, or transmission cycle. The transmission cycle has different elements: The pathogen: the organism causing the infection The host: the infected person or animal ‘carrying’ the pathogen The exit: the method the pathogen uses to leave the body of the host Transmission: how the pathogen is transferred from host to susceptible person or animal, which can include developmental stages in the environment, in intermediate hosts, or in vectors 7 CONTROLLING AND PREVENTING DISEASE The environment: the environment in which transmission of the pathogen takes place. -
Ask a Scientist: How Do People Become Infected with Germs?
One way to think about how living things get sick is to imagine a triangle. The three corners represent the environment... ...the host... All three aspects of this triangle must come ...and the cause of the disease, together for disease to occur. Disease the Agent. agents can be non-infectious or infectious. Non-infectious agents are non-living things that are toxic to the host, like radiation or chemicals... ...while infectious agents are organisms that invade a host to survive. Only infectious agents can spread, or transmit, between hosts. Infectious disease agents, otherwise known as pathogens, A person can become infected with a must infect a host pathogen when in the same environment in order to grow, or as the agent... replicate. Human pathogens, like viruses, bacteria, and parasites, evolved to infect people. Their survival is dependent on quickly invading, making more of themselves, and efficiently transmitting to others. If a pathogen gets past a host’s defenses, it will attempt to infect the host and begin replicating itself. ...and don’t have enough protection in the form The subsequent battle between Many cells will be destroyed as of physical barriers or the germs and the body’s germs kill them through replicating pre-existing immunity. immune system will cause the and as collateral damage from the symptoms of illness. activated immune cells. That’s just how one person gets infected, but how does disease spread? Well, if sick people go around sneezing and coughing without covering their mouth or frequently washing their hands... ...they are actually spreading pathogens all over the environment around them. -
Viral Host-Adaptation : Insights from Evolution Experiments with Phages
This is a repository copy of Viral host-adaptation : insights from evolution experiments with phages. White Rose Research Online URL for this paper: http://eprints.whiterose.ac.uk/77996/ Version: Submitted Version Article: Hall, James Pj, Harrison, Ellie and Brockhurst, Michael A orcid.org/0000-0003-0362-820X (2013) Viral host-adaptation : insights from evolution experiments with phages. Current Opinion in Virology. pp. 572-577. ISSN 1879-6265 https://doi.org/10.1016/j.coviro.2013.07.001 Reuse Items deposited in White Rose Research Online are protected by copyright, with all rights reserved unless indicated otherwise. They may be downloaded and/or printed for private study, or other acts as permitted by national copyright laws. The publisher or other rights holders may allow further reproduction and re-use of the full text version. This is indicated by the licence information on the White Rose Research Online record for the item. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ 1 Viral host-adaptation: insights from evolution experiments with phages 2 James P. J. Hall, Ellie Harrison, Michael A. Brockhurst 3 Department of Biology, University of York, Wentworth Way, York YO10 5DD 4 5 Author for correspondence: 6 Professor Michael A. Brockhurst 7 Postal address: Department of Biology, University of York, Wentworth Way, York YO10 8 5DD 9 Telephone: 00 44 1904 328 576 10 Email: [email protected] 11 12 Abstract 13 Phages, viral parasites of bacteria, share fundamental features of pathogenic animal and 14 plant viruses and represent a highly tractable empirical model system to understand viral 15 evolution and in particular viral host-adaptation. -
Neglected Tropical Diseases in The
Qian et al. Infectious Diseases of Poverty (2019) 8:86 https://doi.org/10.1186/s40249-019-0599-4 SCOPING REVIEW Open Access Neglected tropical diseases in the People’s Republic of China: progress towards elimination Men-Bao Qian1, Jin Chen1, Robert Bergquist2, Zhong-Jie Li3, Shi-Zhu Li1, Ning Xiao1, Jürg Utzinger4,5 and Xiao-Nong Zhou1* Abstract Since the founding of the People’s Republic of China in 1949, considerable progress has been made in the control and elimination of the country’s initial set of 11 neglected tropical diseases. Indeed, elimination as a public health problem has been declared for lymphatic filariasis in 2007 and for trachoma in 2015. The remaining numbers of people affected by soil-transmitted helminth infection, clonorchiasis, taeniasis, and echinococcosis in 2015 were 29.1 million, 6.0 million, 366 200, and 166 100, respectively. In 2017, after more than 60 years of uninterrupted, multifaceted schistosomiasis control, has seen the number of cases dwindling from more than 10 million to 37 600. Meanwhile, about 6000 dengue cases are reported, while the incidence of leishmaniasis, leprosy, and rabies are down at 600 or fewer per year. Sustained social and economic development, going hand-in-hand with improvement of water, sanitation, and hygiene provide the foundation for continued progress, while rigorous surveillance and specific public health responses will consolidate achievements and shape the elimination agenda. Targets for poverty elimination and strategic plans and intervention packages post-2020 are important opportunities for further control and elimination, when remaining challenges call for sustainable efforts. Keywords: Control, Elimination, People's Republic of China, Neglected tropical diseases Multilingual abstracts deprived urban settings [1, 2]. -
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. -
Evolutionary Virology at 40
| PERSPECTIVES Evolutionary Virology at 40 Jemma L. Geoghegan* and Edward C. Holmes†,‡,§,**,1 *Department of Biological Sciences, Macquarie University, Sydney, New South Wales 2109, Australia and †Marie Bashir Institute for Infectious Diseases and Biosecurity, ‡Charles Perkins Centre, §School of Life and Environmental Sciences, and **Sydney Medical School, The University of Sydney, New South Wales 2006, Australia ORCID IDs: 0000-0003-0970-0153 (J.L.G.); 0000-0001-9596-3552 (E.C.H.) ABSTRACT RNA viruses are diverse, abundant, and rapidly evolving. Genetic data have been generated from virus populations since the late 1970s and used to understand their evolution, emergence, and spread, culminating in the generation and analysis of many thousands of viral genome sequences. Despite this wealth of data, evolutionary genetics has played a surprisingly small role in our understanding of virus evolution. Instead, studies of RNA virus evolution have been dominated by two very different perspectives, the experimental and the comparative, that have largely been conducted independently and sometimes antagonistically. Here, we review the insights that these two approaches have provided over the last 40 years. We show that experimental approaches using in vitro and in vivo laboratory models are largely focused on short-term intrahost evolutionary mechanisms, and may not always be relevant to natural systems. In contrast, the comparative approach relies on the phylogenetic analysis of natural virus populations, usually considering data collected over multiple cycles of virus–host transmission, but is divorced from the causative evolutionary processes. To truly understand RNA virus evolution it is necessary to meld experimental and comparative approaches within a single evolutionary genetic framework, and to link viral evolution at the intrahost scale with that which occurs over both epidemiological and geological timescales. -
The Evolution of Life History Trade-Offs in Viruses
Available online at www.sciencedirect.com ScienceDirect The evolution of life history trade-offs in viruses Daniel H Goldhill and Paul E Turner Viruses can suffer ‘life-history’ trade-offs that prevent of trade-offs due to expected pleiotropy (single genes coding simultaneous improvement in fitness traits, such as improved for multiple proteins) and multifunctional proteins that play intrahost reproduction at the expense of reduced extrahost different roles during the viral lifecycle [7]. Viruses tend to survival. Here we examine reproduction-survival trade-offs and have short generation times, large population sizes and ease other trait compromises, highlighting that experimental of culture, allowing efficient experimental evolution studies evolution can reveal trade-offs and their associated that examine life history trade-offs [7]. Whole-genome se- mechanisms. Whereas ‘curse of the pharaoh’ (high virulence quencing easily permits identification of mutations changing with extreme stability) may generally apply for viruses of life history traits, in genome comparisons between ancestral eukaryotes, we suggest phages are instead likely to suffer and evolved viruses. Last, viral protein changes can reveal virulence/stability trade-offs. We examine how survival/ fundamental constraints and biophysical mechanisms of life reproduction trade-offs in viruses are affected by history trade-offs. environmental stressors, proteins governing viral host range, and organization of the virus genome. Future studies In addition, because viruses are exceedingly common on incorporating comparative biology, experimental evolution, earth and affect other organisms in myriad ways [8], and structural biology, could thoroughly determine how viral studying their life history trade-offs illuminates processes trade-offs evolve, and whether they transiently or permanently of global significance.