Viral Replication Cycle

7 Key excerpts on "Viral Replication Cycle"

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  eBook - ePub

  Bacteria and Viruses

  • Britannica Educational Publishing, Kara Rogers(Authors)
  • 2010(Publication Date)
  • Britannica Educational Publishing

    (Publisher)

  CHAPTER 5Cycles and Patterns of Viral Infection

  T he cycles and patterns of viral infection vary depending on the type of virus involved. In order to replicate, however, all viruses must first find a suitable host cell. Whereas some viruses then lie dormant for an indefinite period of time, others set to work appropriating the cells’ genetic replication machinery. The latter is accomplished primarily through the ability of a virus to integrate into host cell DNA. The subsequent manipulation of the host’s genetic machinery results in the generation of numerous viral progeny. When the host cell dies, the progeny are freed to infect new host cells, repeating the infection and replication cycle.

  The mechanisms of viral infection sometimes involve phenomena such as lysogeny, in which a bacteriophage lies dormant within a host bacterial cell and eventually awakens, replicates, and causes the cell to break open (lyse), and malignant transformation, in which animal cells infected with certain viruses are transformed into cancer cells. In addition to cancer, viral infections in humans also underlie various other diseases, ranging from gastrointestinal illness to influenza to AIDS. Thus, the development of vaccines to prevent infection and of antiviral drugs to treat infection form important areas of research at the crossroads of virology and medicine.

  THE CYCLE OF INFECTION

  Viruses can reproduce only within a host cell. The parental virus (virion) gives rise to numerous progeny, usually genetically and structurally identical to the parent virus. The actions of the virus depend both on its destructive tendencies toward a specific host cell and on environmental conditions. In the vegetative cycle of viral infection, multiplication of progeny viruses can be rapid. This cycle of infection often results in the death of the cell and the release of many virus progeny. Certain viruses, particularly bacteriophages, are called temperate (or latent) because the infection does not immediately result in cell death. The viral genetic material remains dormant or is actually integrated into the genome of the host cell. Cells infected with temperate viruses are called lysogenic because the cells tend to be broken down when they encounter some chemical or physical factor, such as ultraviolet light. In addition, many animal and plant viruses, the genetic information of which is not integrated into the host DNA, may lie dormant in tissues for long periods of time without causing much, if any, tissue damage. Viral infection does not always result in cell death or tissue injury; in fact, most viruses lie dormant in tissue without ever causing pathological effects, or they do so only under other, often environmental, provocations.

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  eBook - ePub

  Viruses

  From Understanding to Investigation

  • Susan Payne(Author)
  • 2017(Publication Date)
  • Academic Press

    (Publisher)

  Chapter 3

  Virus Interactions With the Cell

  Abstract

  Virus replication requires specific interactions with host cells. The replication cycle begins with attachment of viral proteins to host cell receptors. The presence or absence of receptors is an important factor in determining if the cell is permissive for infection. The next step in the virus replication cycle is transfer of the genome into cytosol or nucleoplasm. Some viruses transport just their nucleic acid genomes into the cell while others deliver the entire virion. Once in the cell, virion proteins and genome interact with a variety of cell proteins, nucleic acids, and membranes. Productive replication requires synthesis of viral mRNAs, protein, and genomes. The details of these processes vary widely. However, to be successful a virus must be able to compete with host cell for building materials. For example, as the cell is constantly synthesizing proteins, viral mRNAs must be able to redirect ribosomes to their own mRNAs. Some viruses can shut down cellular transcription and translation to redirect those processes to the production of viral proteins. In contrast DNA viruses have developed methods to induce cell DNA replication and/or cell division to obtain materials necessary for genome synthesis. Viruses pack a lot of information into their relatively small genomes. Most do not have the complex promoters that drive cell transcription nor do they have long noncoding introns in their genes. Viruses that replicate in the nucleus often use alternative splicing to generate families of related mRNAs from a single precursor transcript. In other cases a single transcript may be used to produce multiple proteins by ribosome-mediated processes such as leaky scanning, stop codon suppression, and frame shifting. Once viral building blocks have been synthesized, new virions are assembled and must leave the cell. Again, the details of these processes can vary widely. Some of the simplest viruses can assemble in a test tube, from purified capsid proteins and genomes. More complex viruses use a variety of cell proteins and structures for assembly and release.

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  eBook - ePub

  Microbiology

  • Dave Wessner, Christine Dupont, Trevor Charles, Josh Neufeld(Authors)
  • 2016(Publication Date)
  • Wiley

    (Publisher)

  ) , which allows us to determine the burst size, or average number of progeny virions released per infected cell under specified experimental conditions. Of course, genome replication is a critical step in this process, and how genome replication occurs will depend on the type of genome possessed by the virus. Additionally, mRNA that can be recognized and translated by the host cell must be produced. Again, how this mRNA is produced will depend on the type of genome possessed by the virus. These processes together lead to the production of new virus particles, a process collectively referred to as “viral replication.”

  Figure 8.12.

  One-step virus multiplication curve

  By experimentally infecting appropriate host cells in a synchronous fashion, we can observe the kinetics of viral replication and determine the viral burst size, or amount of virus produced from a single infected cell. Following a phase of attachment and entry, the virus enters the latent phase, during which genome replication and protein production occur. During the rise phase, cell lysis and the release of virions begins. The number of extracellular infectious virions eventually reaches a plateau. NOTE: Shown here to illustrate these steps are schematics of E. coli and lambda phage.

  As we mentioned in Section 5.4 , viruses can be classified based on how they replicate or, more precisely, how they generate mRNA. In the Baltimore classification scheme presented here, all viruses are categorized into seven distinct classes:

  • Class I: Double-stranded DNA viruses. DNA serves as a template for synthesis of mRNA. Genome replication usually occurs in the nucleus of the host cell and uses the host DNA-dependent DNA polymerase. Some viruses in this class, like the poxviruses, replicate in the cytoplasm, using viral enzymes.
  • Class II: Single-stranded DNA viruses. Messenger RNA forms from a double-stranded DNA intermediate. Genome replication occurs as the single-stranded genome becomes converted to double-stranded DNA, which then serves as a template for the production of more genomes.
  • Class III: Double-stranded RNA viruses

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  Virus as Populations

  Composition, Complexity, Dynamics, and Biological Implications

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

    (Publisher)

  Villarreal, 2005 , 2008 ; Forterre, 2006a ). Cells are a necessity for viruses and viruses are promoters of cell diversity and, as a consequence, of cellular differentiation (compartmentalization and functional specialization).

  1.7.1 Current Exchanges of Genetic Material

  Present-day viruses reveal several mechanisms of exchange of genetic material that might have roots in early cellular evolution. Temperate bacteriophages (the prototypic example being E. coli phage λ) integrate their genomic DNA in the DNA of their host bacteria. The uptake of cellular genes by viruses has been amply documented in transducing bacteriophages (those that can transfer DNA from one bacterium to another), as well as in RNA and DNA tumor viruses. Even RNA viruses that are not known to include a reverse transcription step in their replication cycle can incorporate host RNA sequences. Replication-competent, cytopathic variants of bovine viral diarrhea virus (a type species of the genus Pestivirus of the important family of pathogens Flaviviridae ) can acquire cellular mRNA sequences in their genome, via nonhomologous recombination (Meyers et al., 1989 ). Insertion of 28S ribosomal RNA sequences into the hemagglutinin gene of influenza virus increased its pathogenicity (Khatchikian et al., 1989 ). Some defective-interfering particles of Sindbis virus included cellular tRNA sequences at their 5′-ends (Monroe and Schlesinger, 1983 ). Sequences related to some flaviviruses can persist in an integrated form into the DNA of the insect vectors Aedes albopictus and Aedes aegypti (Crochu et al., 2004 ). Endogenous hepatitis B viruses (eHBVs) have been identified in the genomes of birds and land vertebrates (amniotes), crocodilians, snakes, and turtles. The evidence is that eHBVs are more than 207 million years old, and that ancient HBV-like viruses infected animals during the Mesozoic Era (Suh et al., 2014 ; Figure 1.4 ). The existence of alternative mechanisms for the integration of viral genetic material into cellular DNA suggests an ancient origin and a selective advantage of exchanges of genetic information in shaping a diverse and adaptable cellular world (Eigen, 1992 , 2013 ; Gibbs et al., 1995 ; Villarreal, 2005 , 2008

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  eBook - ePub

  Introduction to Modern Virology

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

    (Publisher)

  DNA Replication, 2nd edn, revised. W. H. Freeman, San Francisco.
• Liu, H., Naismith, J. H., Hay, R. T. 2003. Adenovirus DNA replication. Current Topics in Microbiology and Immunology 272, 131–164.
• Méndez, J., Stillman, B. 2003. Perpetuating the double helix: molecular machines at DNA replication origins. Bioessays 25, 1158–1167.
• Muylaert, I., Tang, K.-W., Elias, P. 2011. Replication and recombination of herpes simplex virus DNA. Journal of Biological Chemistry 286, 15619–15624.
• Ogawa, T., Okazaki, T. 1980. Discontinuous DNA replication. Annual Review of Biochemistry 49, 421–457.
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Chapter 8 The Process of Infection: IIB. Genome Replication in RNA Viruses

The synthesis of RNA by RNA viruses includes replication, which is defined as the production of progeny virus genomes, and transcription to produce messenger RNA (mRNA). The process of transcription for RNA viruses is described in Chapter 11 where it is discussed in terms of gene expression. This chapter focuses on the process of replication of RNA viruses.

Chapter 8 Outline

1. 8.1 Nature and diversity of RNA virus genomes
2. 8.2 Regulatory elements for RNA virus genome synthesis
3. 8.3 Synthesis of the RNA genome of Baltimore class 3 viruses
4. 8.4 Synthesis of the RNA genome of Baltimore class 4 viruses
5. 8.5 Synthesis of the RNA genome of Baltimore class 5 viruses
6. 8.6 Synthesis of the RNA genome of viroids and hepatitis delta virus

A very large number of viruses have been shown to contain genomes comprised of RNA (Box 8.1). The replication of RNA genomes requires the action of RNA-dependent RNA polymerases which are not encoded by the genome of the infected host cell but instead are synthesized by the virus. During the process of replication of RNA virus genomes, as for all other processes which involve synthesis of nucleic acid, the template strand is ‘read’ by the polymerase travelling in a 3′→5′ direction with the newly synthesized material starting at the 5′ nucleotide and progressing to the 3′ end. Most RNA viruses can replicate in the presence of DNA synthesis inhibitors indicating that no DNA intermediate