Evolution of Viruses

11 Key excerpts on "Evolution of Viruses"

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  Virology

  Principles and Applications

  • John Carter, Venetia Saunders(Authors)
  • 2014(Publication Date)
  • Wiley

    (Publisher)

  The relationships can be portrayed in phylogenetic trees (Section 10.2.1; Figure 21.4). Genome sequencing can ... endless forms most beautiful and most wonderful have been, and are being, evolved. Figure 21.3 Quotation from Charles Darwin's On the Origin of Species (1859). 21.3 Evolution of Viruses 267 also be used to follow changes in rapidly evolving viruses, such as influenza A virus and HIV-1. 21.3.3 Mechanisms of virus evolution In many respects, the underlying processes that drive virus evolution are the same as those that drive the evolution of cellular organisms. These processes involve the generation of genome variants, the vast majority of which are deleterious and do not survive, but a few provide an advantage in a particular niche. For a virus the niche might be a new host species or the presence of an anti-viral drug, and a variant may proliferate in that niche as a new virus strain. Virus genome variants arise as a result of mutations, recombination, reassortment of genome segments, and acquisition of cell genes. Some viruses are able to undergo two or more of these processes. We shall consider each process in turn. 21.3.3.a Mutations When nucleic acids are copied by polymerases some errors are made. If an error is in a protein-coding sequence and if the error results in a change in the amino acid encoded, then the error results in a muta- tion. Natural selection operates and the mutations that survive are those that best fit the virus for its continued survival. There are many selection pressures on viruses. These pressures include the immune response of the host; for example, a new antigenic type of an animal virus that the host’s immune system has not previously encountered is at an advantage compared with anti- genic types against which the host has acquired immu- nity. There is, therefore, heavy selection pressure on virus proteins (e.g. HIV-1 gp120) that are targets of the host’s immune response, and these proteins tend to be the least conserved.

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  Epidemiology

  Current Perspectives on Research and Practice

  • Nuno Lunet(Author)
  • 2012(Publication Date)
  • IntechOpen

    (Publisher)

  Considering a natural transmission cycle of a virus between hosts, maybe involving an invertebrate vector, it is expected that adaptive evolution allows an efficient replication of the virus in such an environment [54]. If the ecosystem is stable and the transmission cycle has been established for a long time, it is expected that the rate of infection and mortality does not critically affect the host population [55]. The genetic background of current viruses evolved in such conditions possibly reflects the interaction of their ancestors with the whole environment, being better explained by an evolutionary ecology approach. Ecology studies contemporary interactions, while Evolutionary Biology is concerned with historical issues. In this sense, Evolutionary Ecology is focused on the integration of these two disciplines to understand the most complicated issues, for example the causes of abundance and distribution of organisms, in relationship with abiotic and biotic dynamical variables [56-58]. Epidemiology – Current Perspectives on Research and Practice 122 VEE studies the impact of the evolutionary response of viruses to the hosts, and other interacting environmental factors, which are shaping their observed diversity and distribution patterns [18]. Although the role of evolutionary processes in driving viruses to new or more severe outcomes of diseases is known, the study of ecological and historical scenario, in which pathogen–host interaction evolves, is not always so well considered. VEE is becoming necessary for understanding and explaining the different patterns of disease in the human population, like acute-to-chronic [59], asymptomatic-to-lethal infections [55, 60] and the emergence of new viruses in humans [61, 62]. Under VEE, the virulence of pathogens is conceived as a process, in which a specific genotype or lineage is selected, which is translated into differential fitness and expansion of the disease [63].

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  Introduction to Modern Virology

  • Nigel J. Dimmock, Andrew J. Easton, Keith N. Leppard(Authors)
  • 2015(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Evolution of any successful parasite has to ensure that the host also survives. The various possible virus–host interactions can be thought of as different ways in which viruses have solved this problem. Introduction to Modern Virology, Seventh Edition. N. J. Dimmock, A. J. Easton and K. N. Leppard. � 2016 John Wiley & Sons, Ltd. Published 2016 by John Wiley & Sons, Ltd. 39 40 Part I The nature of viruses 4.1 Mechanisms of virus evolution Two processes that contribute significantly to virus evolution are recombination and mutation. Mutation involves the well- understood processes that lead to changes in nucleotide sequences in nucleic acids (Fig. 4.1A). Classical recombination takes place infrequently between the single molecule genomes of two related DNA or RNA viruses that are present in the same cell, and generates a novel combination of genes (Fig. 4.1B). Of far greater significance is the potential for genetic exchange between related viruses with segmented genomes. Here, whole functional genes are exchanged, and this type of recombination is called reassortment (Fig. 4.1C). The only restriction for reassortment is the compatibility between the various individual segments making up the functional genome. Fortunately, this seems to be a real barrier to the unlimited creation of new viruses, although it is not invincible since pandemic influenza A viruses can be created in this way (see Section 4.4). When considering virus evolution it is important to appreciate that virus genomes accumulate mutations in the same way as all other nucleic acids and, where conditions enable a mutant to multiply at a rate faster than its fellows, that mutant virus will have an advantage and will predominate in subsequent generations if no additional selective pressures intervene.

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  Virus as Populations

  Composition, Complexity, Dynamics, and Biological Implications

  • Esteban Domingo(Author)
  • 2015(Publication Date)
  • Academic Press

    (Publisher)

  Chapter 7

  Long-Term Virus Evolution in Nature

  Abstract

  Viruses spread to give rise to epidemics and pandemics, and some key parameters that include virus and host population numbers determine virus persistence or extinction in nature. Viruses evolve at different rates of evolution depending on the polymerase copying fidelity during genome replication. Calculated rates of evolution in nature vary depending on the time interval between virus isolations. In particular, intra-host evolution is generally more rapid that inter-host evolution and several possible mechanisms for this difference are considered. The mechanisms by which the error-prone viruses evolve render very unlikely the operation of a molecular clock (constant rate of incorporation of mutations in the evolving genomes). Several computational methods are reviewed that permit the alignment of viral sequences and the establishment of phylogenetic relationships among viruses. The evolution of virus in the form of dynamic mutant clouds in each infected individual, together with multiple environmental influences, render the emergence and reemergence of viral pathogens an unpredictable event, another example of biological complexity.

  Keywords Antigenic diversity Complexity Phylogenetic relationships Rate of evolution Viral disease emergence Virus transmission

  Chapter Contents

  7.1  

  Introduction to the Spread of Viruses. Outbreaks, Epidemics, and Pandemics

    228

  7.2  Reproductive Ratio as a Predictor of Epidemic Potential. Indeterminacies in Transmission Events

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  The Biology of Animal Viruses

  • Frank J. Fenner, B. R. McAuslan, C. A. Mims(Authors)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  INTRODUCTION CHAPTER 17 Evolutionary Aspects of Viral Diseases Viruses are ubiquitous, and have played important roles in the evolution of bacteria, plants, and animals. In the first place, infectious diseases in themselves have been powerful selective forces, whose role has been well demonstrated, for example, with malaria and the human genes for hemoglobin S and glucose-6-phosphate de-hydrogenase deficiency. Speculatively, both DNA and RNA viruses may also have played a part in producing the increase in cellular DNA that has charac-terized evolutionary progress, by transduction or integration, directly or through the intervention of the reverse transcriptase. Viruses themselves are also subject to natural selection. There is no fossil record of the viruses, but clues about the antiquity of some existing viruses may be obtained from biogeographical observations, or by study of the distribution of members of different viral genera throughout the animal or plant kingdoms. In a few situations it has been possible to witness evolution in action, with viruses and their vertebrate hosts. Man's disturbances of the biosphere, and some medical innovations, have created new viral diseases for man himself and for his domesticated animals. Rapidly increasing urbanization, and the swift and large-scale movement of human beings over the whole world, have led to a well-nigh universal distribu-tion of the human viruses, thus changing radically epidemiological patterns that evolved in small, relatively isolated human communities. THE ANTIQUITY OF SOME VIRUSES All viruses depend for their replication on the energy sources, the ribosomes and some of the enzymes of their host cells. They must therefore have evolved after cells and be derived from them, either by the parasite degeneration of Green and Laidlaw or by the sequestration of fragments of cellular nucleic acid and its acquisition of the capacity to infect other cells (see Chapter 1).

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  Principles of Virology, Volume 2

  Pathogenesis and Control

  • S. Jane Flint, Vincent R. Racaniello, Glenn F. Rall, Anna Marie Skalka, Theodora Hatziioannou(Authors)
  • 2020(Publication Date)
  • ASM Press

    (Publisher)

  The word “evolution” conjures up images of fossils, dusty rocks, and ancestral phylogenetic trees, covering eons. Thanks to the recent development of rapid sequencing methods, we can now discover fossils of ancient viruses, not in rocks, but in the DNA of living organisms. For currently circulating viruses, evolution is not only contemporary (and rapid), but also has profound effects on both viruses and their hosts: as host populations change or become resistant to infection, viruses that can overcome such changes are selected. Viral infections can also exert significant selective forces on the survival and evolution of host populations. In some ways, viral evolution can be thought of as the product of a continuing arms race in which both viral and host cell genes are selected in response to the pressures encountered during infection.

  How Do Virus Populations Evolve?

  A large, genetically variable host population dispersed in everchanging environments may appear to present insurmountable barriers to the survival of viruses, yet viruses are plentiful and ubiquitous. The primary reason for this remarkable success is that virus populations display spectacular genetic diversity, manifested in the large collections of genome permutations that are present in a population at any given time. The sources of such diversity are mutation, recombination, and reassortment of viral genes.

  Virus evolution

  is driven by selective pressure acting on diversity that promotes survival of genomes with the most advantageous properties.

  In most viral infections, hundreds to thousands of progeny particles are produced after a single cycle of reproduction in one cell. When genome copying is error-prone, almost every new virus particle can differ from every other. Consequently, it is misleading to think of an individual particle as representing an average for that population. This great diversity in the virus population provides avenues for survival under varying conditions. Every individual virion is a potential winner, and occasionally, the rarest genotype in a particular population will be the most common after a single selective event.

  Positive and negative selection of preexisting genotypes in a population can occur at any step in a viral life cycle. The requirement to spread within an infected host, as well as between hosts, exposes virus particles to a variety of host antiviral defenses. In addition, the density of host populations, their social behavior, and their health represent but a few of the other forces that can affect the survival of virus populations.

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  Viruses

  Agents of Evolutionary Invention

  • Michael G. Cordingley(Author)
  • 2017(Publication Date)
  • Harvard University Press

    (Publisher)

  Evolutionary Mechanisms of DNA Viruses · 139 herpesviruses is measured differently from that of poxviruses. Herpesvi-ruses persist in their host after acute infection in order to enlarge the time window in which they can continue to replicate and be transmitted to new hosts. For these viruses it is advantageous to evolve a stable entente with their host to promote the propagation of their genetic information. They have minimized the necessity for rapid evolutionary change by coevolving over millennia in lockstep with their hosts. Poxviruses require that acute symptomatic infections of the host sustain their epidemic spread in the population and successful lineages expand their host range and move into new species. Poxviruses are in the evolutionary fast lane. They must remain evolutionarily agile and possess the ability for rapid genetic innovation. These qualities are essential for them to compete with their evolving hosts and to move successfully between host species, a modus operandi most often associated with RNA viruses. Poxvirus Party Tricks The most important field of conflict between a virus and its host is where the host defense mechanisms meet the virus’s tools for immune evasion. This interface is often based in physical interactions that take place between viral proteins and cellular proteins under intense selective pres-sure. It is evident in positive selection on viral genes, such as the immune selection of influenza HA epitopes, and also on the genes of the host cell. In a tit-for-tat competition, the cellular genes responsible for controlling virus infection and the corresponding viral genes directing immune eva-sion each strive to gain the upper hand. Examination of Red Queen con-flicts that have driven genetic innovation and adaptive evolution of virus and host genes alike gives evolutionary biologists a ringside seat to observe the evolutionary arms race between hosts and pathogens.

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  Origin and Evolution of Viruses

  • Esteban Domingo, Robert G. Webster, John F. Holland(Authors)
  • 1999(Publication Date)
  • Academic Press

    (Publisher)

  Those viral-like sequences remain- ing in their host now seem like remnants, whose original impact can only dimly be surmised. Furthermore, such data are unlikely to provide any information concerning what may have been major biological events mediated by virus. For example, the potential termination of a species by virus epidemic would leave no trace in the current genetic record. In addition, evolu- tionary science, whose conceptual synthesis in the 1930s (Dobzhansky, 1937) preceded the modern understanding of a virus as a molecular genetic parasite in the 1950s (Luria, 1959), has yet to fully appreciate the contributions of viral molecular genetic parasites and horizontal gene flow to host evolution, especially those of per- sistent or inapparent infections. This chapter considers the evolution of DNA viruses as a separate topic. Most reviews on virus evolution have concentrated on RNA viruses with their correspondingly high muta- tion rates and genetically heterogeneous popu- lations (Domingo et al., 1996; Domingo and Holland, 1997; Garnett and Antia, 1998). The apparent genetic stability of DNA viruses makes them appear to evolve slowly and thus they have received much less attention. However, DNA viruses (and retroviruses) tend to have a very intimate molecular relationship with their Origin and Evolution of Viruses ISBN 0-12-220360-7 391 Copyright 9 1999 Academic Press All rights of reproduction in any form reserved. 392 L.P. VILLARREAL host. As host genomes are DNA and as DNA replication is tightly regulated, DNA viruses must either parasitize this host DNA replication apparatus or override host regulation with viral replication proteins. DNA viruses therefore face common mechanistic problems that can require a very specific involvement with host molecular genetic function, which constitutes the viral habitat.

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  Viruses

  A Natural History

  • Marilyn J. Roossinck(Author)
  • 2023(Publication Date)
  • Princeton University Press

    (Publisher)

  Fourthly, and finally, viruses that jump into novel hosts may show a very rapid rate of evolution as they adapt to a different environment. This type of dramatic change is uncommon in cellular life.  An artist’s rendition of a mutated coronavirus (in blue) exiting an infected cell. 140 E V O L U T I O N The concept of biological fitness is simple: an individual that is more fit, that is well adapted and healthy within its environment, will produce more offspring and these will be more likely to survive, compared to an individual that is less fit. Measuring fitness is not so simple, however, and nor is understanding how fitness evolves. Fitness 141 F I T N E S S Clearly, if a virus mutates and that mutation makes it able to replicate faster or transmit better, then the virus would be more fit. However, there are limits to this. If the virus also makes its host very sick, then that can be detrimental to its fitness in the long run. For example, if you have a flu virus that replicates very rapidly such that you have a lot of virus coursing through your body, you are probably going to feel pretty bad and are most likely going to stay home in bed. That isn’t very good for the virus, because you aren’t going out and letting it spread to other hosts. Instead, it might be better for the virus to make you less sick. If this means the virus can’t replicate to such high levels, it may evolve to some intermediate level, where it replicates well enough to make a lot of copies of itself, but not so well that it makes you too sick to get out and about. Many viruses are most transmissible early in infection. If this stage happens ahead of symptoms then it is an advantage for the virus, as the host will be mingling with many susceptible hosts. It is possible that viruses become less transmissible over the course of an infection because of the accumulation of deleterious mutations.

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  Aspects of Cell Regulation

  • G. H. Bourne, J. F. Danielli, G. H. Bourne, J. F. Danielli(Authors)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  It was accepted that the group belonged with the bacteria and not the viruses. This decision made the gap between bacteria and viruses much more evident. Lwoff (1957) wrote in his lecture on 'The concept of virus, Viruses should be considered as viruses because viruses are viruses. III. Mechanisms for Change in Viruses Work over the past three decades has shown that viruses possess a variety of mechanisms by which genetic change can take place. These are summarized briefly below. A. MUTATION DUE TO A BASE CHANGE Single base change mutations are a common cause of variability among vi-ruses. Stable misincorporation of a nucleotide during cellular DNA replication occurs with a frequency of only 10~ 7 -10~ K) mutations per nucleotide pair synthesized (Mildvan and Loeb, 1979). This fidelity has been attributed to the proof reading exonuclease and repair function of prokaryote DNA poly-merases and to the activities of other proteins associated with the DNA poly-merases of eukaryotes (Kunkel and Loeb, 1981). The error rate in RNA synthesis is several orders of magnitude higher. Domingo et al. (1978) estimated from their nucleotide sequence data that in a multiply passaged QB bacteriophage population almost all of the particles have a base sequence differing from the wild-type sequence in at least one residue. A heterogeneous population of this kind should be capable of rapid change in a changing environment. Under standard growth conditions the mutations cause a lowered growth rate compared with wild type. Thus it seems probable that any stock culture of a virus with an RNA genome will contain a large pool of base change mutants. In the protected environment provided by latent or persistent infections, it has been demonstrated for RNA viruses in both vertebrates (Holland et al., 1979) and fungi (Kane et al., 1979) that divergence of base sequence from the original parental type can be very rapid.

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  Viruses, Evolution and Cancer Basic Considerations

  • Edouard Kurstak(Author)
  • 2012(Publication Date)
  • Academic Press

    (Publisher)

  PART VII VIRUSES AND THEIR EVOLUTION This page intentionally left blank C H A P T E R 2 0 Visualization of the Evolution of Viral Genomes WAC LAW SZYBALSKI AND ELIZABETH H. S ZY ΒA LS ΚI I. Introduction 563 II. Reducing the Genome Size 566 A. Deletions 566 B. Substitutions 567 III. Increasing the Genome Size 568 IV. Shortening the Intergene Distance 569 A. Deletions 569 B. Inversions 570 C. Translocations 570 V. Insertosomes 570 VI. Acquiring a New Function 572 A. Insertions 572 B. Deletions 572 C. Substitutions 573 VII. Hybrid Phages 574 VIII. Plasmids 575 IX. Conclusions 577 X. Summary 580 References 580 I. Introduction The evolution of viral genomes proceeds by mutation and genetic recombination. Until recently, most of our knowledge on mutation and recombination was derived from genetic analysis. We shall be concerned here mainly with the complementary approach of physical mapping by electron micrography of heteroduplex D N A , according to the form-amide technique developed by Westmoreland et al. (1969). This 563 564 WACLAW SZYBALSKI AND ELIZABETH H. SZYBALSKI method readily permits the detection and precise localization of genetic changes that involve more than 10 to 50 nucleotide pairs, but in its simple form is not suited for detecting point mutations and rearrang-ments encompassing shorter sequences. In brief, the principle of the technique is as follows. When a separated D N A strand from a particular viral strain is annealed in 5 0 % formamide solution with a complementary strand from a genetically different mu-tant, the regions of sequence homology form duplex D N A , whereas the heterologous segments remain single stranded, within the defined het-eroduplex molecule. The D N A is spread on the surface of distilled water in a cytochrome c matrix, according to the basic protein mono-layer technique of Kleinschmidt and Zahn (1959), and finally visualized by electron microscopy and the contour lengths measured photoop-tically.

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