Latent Viruses

5 Key excerpts on "Latent Viruses"

• 

  eBook - ePub

  Introduction to Modern Virology

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

    (Publisher)

  + T lymphocytes per person may be infected in this way. The latent virus can reactivate at any time though the stimuli for this are not well understood. This is important as most active virus multiplication, but not the latent virus infection, can be eliminated by chemotherapy (see Section 21.6). Thus, the latent infection acts as a reservoir from which virus can reappear if antiretroviral therapy is stopped. When this occurs, the levels of infectious virus in the body often exceed those prior to the treatment and there is a greatly enhanced likelihood of drug-resistant viruses appearing due to selection pressures. This means that the current therapy regime has to be maintained for life, with the attendant difficulties of expense, toxicity, non-compliance, or the eventual breakthrough of resistant mutants.

  Key Points

  • Latency is an outcome of infection for certain viruses and is a state defined by the presence of viral genome without the production of infectious virus, but in which it is possible to reactivate a lytic infection.
  • Among animal viruses, all herpesviruses have the ability to establish latent infections.
  • The pattern of gene expression during latency is different to that seen during an acute infection: fewer virus genes, and sometimes no genes, are expressed during latency.
  • In phage λ the establishment of latency is determined by a balance between the action of gene activators and gene repressors.
  • In HSV-1 only RNA from the LATs and micro RNAs are seen during latency. In the other herpesviruses, several virus proteins may be produced during latency.
  • Latency requires suppression of the early steps in the cascade of lytic gene expression.
  • Following reactivation, infectious virus is produced from latently infected cells.
  • In animals, the immune system is key in dealing with reactivation of infection.

  Questions

  • Consider the control of lysogeny in bacteriophage lambda and compare this with the gene expression of herpesviruses during the establishment and maintenance of latency.
  • Discuss the potential outcomes of infection of humans with herpesviruses and describe the processes which control and determine the various stages of the infection.

  Further Reading

  1. Johnson, A. D., Poteete, A. R., Lauer, G., Sauer, R. T., Ackers, G. K., Ptashne, M. 1981. λ repressor and cro-components of an efficient molecular switch. Nature (London)

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  eBook - ePub

  The Molecular Biology of Neurological Disease

  Butterworths International Medical Reviews

  • Roger N. Rosenberg, A. E. Harding(Authors)
  • 2013(Publication Date)
  • Butterworth-Heinemann

    (Publisher)

  16

  Detection of viral genes in neurological disease

  R.F. Itzhaki

  Publisher Summary

  This chapter focuses on the detection of viral genes in neurological disease. Before a role can be ascribed to viruses in certain neurological diseases, more information is needed about persistence and latency, particularly the effect on host cells and the mechanisms of reactivation of latent genome at the molecular level. Of all the results so far obtained, one of the most intriguing is the detection of viral sequences in normal brain and in certain diseased brains. In the case of herpes simplex virus (HSV), this is perhaps not surprising as about one-third of the population suffer reactivation because of factors such as stress, sunlight, and menstruation. Possibly many other people harbor HSV or other viral genomes but can keep the virus quiescent either because of a more efficient immune system or through genetic or environmental factors unfavorable to reactivation. In contrast, others may be particularly prone to repeated bouts of reactivation, and if especially susceptible regions of brain are affected, these could cumulatively produce neurological dysfunction.

  INTRODUCTION

  This chapter is concerned with persistent and latent viral infections, excluding those due to RNA tumour viruses. These topics are both fascinating and challenging but are far less well understood than acute infections. Definitions of persistence and latency have not been standardized. Persistence is sometimes equated with chronic or dynamic latency and usually includes the category of slow infection; latency is sometimes treated as synonymous with persistence but is occasionally classed as a subcategory of the latter. However, in general, and in this chapter, persistent or chronic infection is defined as that where there is continuous production, although at a very low level, of the virion. In contrast, in latent infection, no virion is produced and production of viral messenger RNA (mRNA) and of viral protein is low or zero, but the viral genome is maintained in the host cell, either integrated within the cell genome or in episomal form.

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  eBook - ePub

  Viral Immunology and Immunopathology

  • Abner Louis Notkins(Author)
  • 2014(Publication Date)
  • Academic Press

    (Publisher)

  A number of virus infections of man and of animals persist for months, years, or for the lifetime of the infected host, and such infections have many different patterns of interaction with the host. Some persistent infections result in high levels of virus in the tissues and serum, and sometimes excreta of the infected host. Infections of this type may cause serious or fatal disease or may be largely or even completely silent. Other infections, particularly those of the herpesvirus group, are characterized by long periods of latency and brief episodes of viral activation, usually accompanied by clinical disease. Still other infections result in long-term persistence of very low titers of virus in tissues, usually with no accompanying physiologic abnormality or disease. The infected host has a number of different defense mechanisms, among which are cellular and humoral immunity, which may limit the period or extent of infection. Conversely, viruses have means of spread and ways of eluding host responses that tend to reduce the effectiveness of these defenses. In this article I shall discuss the mechanisms of viral persistence in the presence of host immunity.

  A large number of host determinents may contribute to the persistence of viral infection and the production of lesions. Such host factors include age, genetic factors, the degree of maturity and competence of the immunologic system, the cell types infected by the virus, and the presence of underlying diseases. Important viral determinents include the method by which the virus spreads, the antigenicity of the virus, the physical form of the virus, formation of defective or partially defective viral particles, and occasionally direct effects of the virus on the immune system. Such host and viral factors dynamically interact and will be discussed using specific examples of persistent infection.

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  eBook - ePub

  Plant Virus-Host Interaction

  Molecular Approaches and Viral Evolution

  • R.K. Gaur, Pradeep Sharma, Thomas Hohn(Authors)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  Chapter 14

  Diversity of latent plant–virus interactions and their impact on the virosphere

  K.R. Richert-Pöggeler,    Institute for Epidemiology and Pathogen Diagnostics, Julius Kühn-Institut, Braunschweig, Germany

  J. Minarovits,    University of Szeged, Faculty of Dentistry, Department of Oral Biology and Experimental Dental Research, Szeged, Hungary

  Abstract

  Viruses and viroids that are not causing symptoms on their initial host plant are described by the terms ‘latent,’ ‘cryptic,’ or ‘symptomless,’ and they represent 7% and 4% of the classified plant viruses and viroids, respectively. Additionally, endogenous plant pararetroviruses that reside in their host genome are often dormant and therefore asymptomatic. Improved sequencing and diagnostic technology has demonstrated that viral sequences are ubiquitously present in the biosphere even if the signs or symptoms of infection are not obvious. Accordingly, the number of latent plant viruses listed today does not reflect the true range of Latent Viruses existing in plants. Biodiversity within the virosphere comprises virus–host, virus–vector, virus–virus, and virus–viroid interactions. Invasion of new host plants, climatic changes, and changes in plant production and distribution can have a major impact on symptomatic outbreaks of otherwise Latent Viruses. Here we describe, for selected ornamentals, how these changes can induce Latent Viruses, and we report on possible underlying biochemical mechanisms. Comparison of virus latency in plant and animal hosts indicates that epigenetic modifications are an important factor for regulation in both systems.

  Keywords

  Latent Viruses; ornamental plant viruses; epigenetic regulation; endogenous pararetrovirus; herpesvirus; retrovirus

  Acknowledgments

  We thank K Kobayashi, B Poeggeler, W Menzel, and T Kühne for stimulating discussions and valuable comments. We thank M Wassenegger for viroid analysis in S. jasminoides . We thank C Maaß and S Schuhmann for expert technical assistance, and C Maaß for photography of S. jasminoides

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  eBook - ePub

  Molecular Biology

  • David P. Clark(Author)
  • 2009(Publication Date)
  • Academic Cell

    (Publisher)

  intracellular parasites ; that is to say that they must actually enter the cells of the host organism to replicate. Note that not all intracellular parasites are viruses. Certain disease-causing bacteria and protozoans may enter the cells of higher organisms and live inside them as parasites. However, these parasites are nonetheless living cells themselves and contain their own ribosomes to make their own proteins. This chapter does not attempt to cover the realm of virology systematically. Rather, examples are given to illustrate novel aspects of molecular biology found among the viruses.

  Life Cycle of a Virus

  A virus alternates between two forms, an inert virus particle, the virion, which survives outside the host cell, and an active intracellular stage. The life cycle of a typical virus goes through the following stages (Fig. 17.03 ):

  a. Attachment of virion to the correct host cell b. Entry of the virus genome c. Replication of the virus genome d. Manufacture of the virus proteins e. Assembly of new virus particles (virions) f. Release of new virions from the host cell

  Figure 17.03 Virus Life CycleThe life cycle of a virus starts when the viral DNA or RNA enters the host cell. Once inside, the virus uses the host cell to manufacture more copies of the virus genome and to make the protein coats for assembly of virus particles. Once multiple copies of the virus have been assembled, the host cell is burst open to allow the viral progeny to escape and find new host cells to infect.

  Virus genes subvert the host cell into manufacturing more virus particles.

  Attachment of a virus requires a protein on the virus particle to recognize a molecule on the surface of the target cell. Sometimes this receptor is another protein; sometimes it is a carbohydrate. Often it is a glycoprotein, that is a protein with carbohydrate groups attached. On some virus particles, the recognition proteins form spikes or prongs sticking out from the surface. Most bacterial and plant viruses abandon their protein coat when they infect a new host cell. Only the genetic material (DNA or RNA) enters the cell. Animal viruses vary in regard to when exactly they disassemble their protein coat.

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