Viral Mutations

6 Key excerpts on "Viral Mutations"

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  Point Mutation

  • Colin Logie(Author)
  • 2012(Publication Date)
  • IntechOpen

    (Publisher)

  Part 2 Point Mutation in Viruses: From Drug Resistance to Vaccination 4 Point Mutations and Antiviral Drug Resistance José Arellano-Galindo 1 , Blanca Lilia Barron 2 , Yetlanezi Vargas-Infante 3 , Enrique Santos-Esteban 4 , Emma del Carmen Herrera-Martinez 5 , Norma Velazquez-Guadarrama 1 and Gustavo Reyes-Teran 6 1 Laboratorios de Virología y Microbiología Hospital Infantil de México Federico Gómez, 2 Head of laboratory of Virology Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional, 3 Internal Medicine/Infectious Diseases/HIV, Centro de Investigación en Enfermedades Infecciosas Instituto Nacional de Enfermedades Respiratorias, Nacional de Enfermedades Respiratorias 4 Departamento de Bioquimica Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional, 5 Academisian of Facultad de Ciencias de la Salud Universidad Anahuac, Mexico Norte 6 Head of Department, Centro de Investigación en Enfermedades Infecciosas Instituto Nacional de Enfermedades Respiratorias, México 1. Introduction Viruses are the most abundant biological entities on the planet and their life cycles include the infection of other organisms. Although the presence of viruses is obvious in host organisms that show signs of disease, many healthy organisms are also hosts of non-pathogenic virus infections, where some are active and others are quiescent. It is doubtless that the known viruses represent only a tiny fraction of the viruses on Earth. There is a strong correlation between how intensively a species is studied and the number of viruses found in that species. Our own species is the subject of the most attention, because we have the greatest interest in learning about agents and processes that affect our health. If other species received the same amount of attention, it is likely that many would be found to be hosts to similar numbers of viruses (Breitbart et al., 2005).

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  Virus as Populations

  Composition, Complexity, Dynamics, and Biological Implications

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

    (Publisher)

  The potential for genetic variation of RNA and DNA viral genomes is remarkable, and it is the ultimate molecular mechanism that lies at the origin of the virus diversity delineated in Chapter 1. 2.2 Molecular Basis of Mutation Mutation is a localized alteration of a nucleotide residue in a nucleic acid. It generally refers to an inheritable modification of the genetic material. In the case of viral genomes, mutations can result from different mechanisms: (i) template miscopying (direct incorporation of an incorrect nucleotide); (ii) primer-template misalignments that include miscoding followed by realignment, and misalignment of the template relative to the growing chain (polymerase “slippage” or “stuttering”); (iii) activity of cellular enzymes (i.e., deaminases), or (iv) chemical damage to the viral nucleic acids (deamination, depurination, depyrimidination, reactions with oxygen radicals, direct and indirect effects of ionizing radiation, photochemical reactions, etc.) (Naegeli, 1997 ; Bloomfield et al., 2000 ; Friedberg et al., 2006). The basis of nucleotide misincorporation during template copying lies mainly in the electronic structure of the bases that make up DNA or RNA. Each base in DNA (adenine, A; guanine, G; cytosine, C; thymine, T) and RNA (with uracil, U instead of T) includes potential hydrogen-bonding donor sites (amino or amino protons) and hydrogen-bonding acceptor sites (carbonyl oxygens or aromatic nitrogens) that contribute to standard Watson-Crick base pairs (Figure 2.1) as well as wobble base pairs (nonstandard Watson-Crick, but fundamental for RNA secondary structure and mRNA translation) (Figure 2.2). The conformation of the purine and pyrimidine bases is highly dynamic. Amino and methyl groups rotate about the bonds that link them to the ring structure

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  Emerging Neurological Infections

  • Christopher Power, Richard T. Johnson, Christopher Power, Richard T. Johnson(Authors)
  • 2005(Publication Date)
  • CRC Press

    (Publisher)

  This chapter addresses the molecular mechanisms of genetic variation of pathogens and some biological implications of pathogen variation related to disease emer-gence, with emphasis on highly variable RNA viruses, the source of many emer-gent and reemergent diseases covered in this book. It must be stressed, however, that the general principles that govern the adaptive dynamics of all types of pathogens are of a similar nature (8,22–24). 2. THE EVOLUTION OF MICROBIAL PATHOGENS Evolutionary processes are amenable to experimental analysis with microbial pathogens because of their rapid replication and in many cases the frequent occurrence of genetic changes and adaptive responses to designed environments. 4 Domingo In contrast, minimal evolutionary processes in differentiated organisms very often take a long time under laboratory conditions. Microbes have become ideal objects for experimental studies on evolution. 2.1. Mutation Rates of Cells, Viruses, and Intracellular Genetic Elements The main mechanisms of genetic variation are mutation, several classes of genetic recombination, and chromosome or genome segment reassortment (Fig. 2). Drake (25) estimated mutation rates for some bacteria and bacteriophages (viruses which infect bacteria) that have DNA as their genetic material. From the frequency of reversion of conditionally lethal mutations, mutation rates of 2 × 10 -10 substitutions per nucleotide copied were estimated for Escherichia coli and Salmonella Microbial Evolution and Emerging Diseases 5 Figure 2 Schematic representation of some types of genetic modifications that underlie or affect adaptability of pathogens. (A) Mutation: Symbols on progeny genome indicate different types of mutations. (B) Homologous recombination. (C) Genome segment reas-sortment. (D) Nonhomologous recombination. (E) Intracellular transposition or rearrange-ment of genetic material.

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  Basic Virology

  • Edward K. Wagner, Martinez J. Hewlett, David C. Bloom, David Camerini(Authors)
  • 2009(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Still, the basic strategy behind such molecular manipulation is based on only a few basic principles of molecular biology – the characterization of viral genomes and gene products that has been described in Part III. Now, with the application of this information to the replication strategies of the major groups of viruses described in Part IV, we can illustrate both methods for manipu- lating viral genomes and for determining the effects of such manipulation of the parameters of viral infection. Lasting sequelae (cancer/degenerative conditions) Slow evolution Genome Protein function Replication (cell and organism) Defense Disease Genome Protein function Replication Recovery and immunity Evolution Exploitation Molecular knowledge Molecular knowledge Host Virus Maintenance Fig. 22.1 The impact of molecular understanding of viral and host genes on the interactions between virus and host. Different stages of the virus replication cycle and the interaction between virus and host are illustrated along with the outcomes of such interactions. Understanding the molecular basis of such interactions are important in controlling disease, aiding recovery and immunity, prevention of lasting sequelae. These interactions also can be exploited in biotechnology and medicine. CHAPTER 22 THE MOLECULAR GENETICS OF VIRUSES 437 Mutations in genes and resulting changes to proteins Sometimes, as nucleic acids replicate, a mistake occurs. This is a very rare event in organisms, but in viruses that replicate so rapidly and whose replication enzymes are often error-prone, such changes occur with appreciable frequency. With some viruses that have RNA genomes, such as HIV, the polymerase can generate one mistake for every 10,000 bases transcribed so that many changes are generated. Indeed, as outlined in Chapter 20, Part IV, some of these changes have a role in the virus’ ability to avoid the body’s immune defenses.

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  Viruses

  A Natural History

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

    (Publisher)

  These random changes can happen almost anywhere in the genome, although in cells they are more likely in active areas where transcription to RNA or copying of the DNA is taking place. In cells, most of these mistakes are corrected by enzymes that recognize them as such and cut out the bad DNA, replacing it with the correct DNA. Only rarely do mutations remain in the genome. To be passed on to the next generation, mutations have to occur in germ-line cells, such as eggs or sperm.  Charles Darwin (1809–1882) traveled around the world on board HMS Beagle as the ship’s naturalist. On his journey, especially in South America, his observations led him to develop his hypothesis of evolution. 137 138 E V O L U T I O N Viruses evolve through natural selection too, just like all other gene-based entities. However, they face some different constraints.Viruses often have overlapping genes, so a single nucleotide mutation can impact more than one protein. In RNA viruses there is a lot of biological activity in the way the RNA folds, and this is dependent on the nucleotide sequence of the RNA. This means that natural selection can be important outside of the constraints of protein coding. Mutations become important when food sources or the environment change. For example, let’s say you have a mutation that allows you to tolerate heat better than most people. As the climate changes and temperatures increase, your offspring will be more likely to survive and prosper than those who cannot tolerate higher temperatures. However, if the climate were to get colder, your offspring would not have any advantage. This is the essence of natural selection, the theory of evolution described by Darwin. Accumulation of mutations during replication On average, an RNA virus might make a mistake, or mutation, about once every time it copies its genome.

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  Animal Virus Genetics

  • Bernard N. Fields, Rudolf Jaenisch, Bernard N. Fields, Rudolf Jaenisch(Authors)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  The advantages of multiple, but more subtle mutational adaptions may be of equal evolutionary importance for viruses, both in acute and persistent infection. JOHN HOLLAND et al. ACKNOWLEDGEMENTS We thank Estelle Bussey for excellent technical assistance· REFERENCES I. Stevens, J., Todaro, G., and Fox, CF., Eds· (1978). Persistent Viruses. Academic Press, New York. 2o Preble, O.T., and Youngner, J.S. (1973). J_. Virol. 2j 472. 3. Fields, B.N., and Raine, C.S. (1974). In Mechanisms of Viral Diseases, C.F. Fox, ed. W.A. Benjamin, Menlo Park, pp. 161. 4. Youngner, J.S. Dubovi, J., Quagliana, D.O., Kelley, M., and Preble, O.T. (1976). £. Virol. ±, 90. 5. Wagner, R.R., Levy, A., Snyder, R., Ratcliff, G., and Hyatt, D. (1963). J_. Immunol. 9J_, 112. 6. Ramseur, J.M. and Friedman, R.M. (1977). J_. Gen. V i ro I. 37, 523. 7. Huang, A., and Baltimore, D. (1970). Nature 226, 325. 8. Holland, J.J., and Villarreal, L.P. (1974). Proc. Natl. Acad. Sei. U.S.A. 71, 2956. 9. Roux, L., and Holland, J.J. (1979). Virology 93, 91. 10. Ahmed, R., and Graham, A.F. (1977). J_. Virol. 23, 250. 11. Welsh, R.M., and Oldstone, M.B.A. (1977). J_. Exp. Med. 145, 1449. 12. Kawai, A., Matsumoto, S., and Tanabe, K. (1975). Virology 67, 520. 13. Popescue, M., and Lehmann-Grube, F. (1977). Vi roIogy 77, 78. 14. Schmaljohn, C., and Blair, CD. (1977). J_. Virol. 24, 580. 15. Weiss, B., Rosenthal, R., and Schlesinger, S. (1980). J_. Virol. 33_, 463. 16. Nishiyama, Y., Ito, Y., and Shimokata, K. (1978). J_. Gen. Virol. 40, 481. 17. Stinski, M.F., Mocarski, E.S., and Thomsen, D.R. (1979). L· Virol. 3^ 231. 18. Henry, B.E., Newcomb, W.W., and 0 f Cal lagharr, D.J. (1979). Virology 92, 495. 19. Norkin, L.C (1979). Virology 95, 598. 20. Holland, J.J., Grabau, E.A., Jones, C.L., and Semler, B.L. (1979). Cell 16, 495. 708 59. VIRAL MUTATION IN PERSISTENT INFECTION 709 21. Prîngle, C.R.

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