Viral Replication

10 Key excerpts on "Viral Replication"

• 

  eBook - PDF

  Introduction to Modern Virology

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

    (Publisher)

  1.3 The virus multiplication cycle We now know a great deal about the processes which occur during the multiplication of viruses within single cells. The precise details vary for individual viruses but have in common a series of events marking specific phases in the multiplication cycle. These phases are summarized in Fig. 1.2 and are considered in detail in Part II of this book. The first stage is that of attachment when the virus attaches to the potential host cell. The interaction is specific, with the virus attachment protein(s) binding to target receptor molecules on the surface of the cell. The initial contact between a virus and host cell is a dynamic, reversible one often involving weak electrostatic interactions. However, the contacts quickly become much stronger with more stable interactions which in some cases are essentially irreversible. The attachment phase determines the specificity of the virus for a particular type of cell or host species. Having attached to the surface of the cell, the virus must effect entry to be able to replicate in a process called penetration or entry. Once inside the cell, the genome of the virus must become available. This is achieved by the loss of many, or all, of the proteins that make up the particle in a process referred to as uncoating. For some viruses, the entry and uncoating phases are combined in a single process. Typically, these first three phases do not require the expenditure of energy in the form of ATP hydrolysis. Having made the virus genome available it is now used in the biosynthesis phase when genome replication, transcription of mRNA and translation of the mRNA into protein occur. The process of translation uses ribosomes provided by the host cell and it is this requirement for the translation machinery, as well as the need for molecules for biosynthesis, that makes viruses obligate intracellular parasites. The newly-synthesized

  Sign up to read

  Learn more about book
• 

  eBook - ePub

  Animal Cell Technology

  From Biopharmaceuticals to Gene Therapy

  • Leda Castilho, Angela Moraes, Elisabeth Augusto, Mike Butler(Authors)
  • 2008(Publication Date)
  • Taylor & Francis

    (Publisher)

  For a better understanding of the pathological effects caused by viral infections and of their control by vaccination or antiviral therapy, it is important to understand how viruses infect cells, express their genes, multiply, and change the cellular metabolism after the infection. The genetic characteristics of the host as well as its sensitivity, are factors that must be considered in evaluating the magnitude of Viral Replication.

  Viruses are exclusively intracellular organisms and therefore depend on the cells to multiply. A complete viral particle, or virion, consists of one nucleic acid molecule (RNA or DNA) covered by a protein layer (nucleo-capsid). Some virions have a lipid cover with a glycoprotein envelope. The main function of the virion is to transport the viral genome to the interior of the host cell to be replicated and amplified.

  The infectivity of host cells varies considerably between viruses. A specific virus may have a great diversity of host cells, while another may be capable of infecting only one type of cell. The sensitivity defines the capacity of the cell or animal to be infected.

  Viral multiplication involves different ways of replication. However, there are some common characteristics in the replicative cycles of viruses. Initially, viruses insert their genetic material (RNA or DNA) into the cell, and the size, composition, and genetic organization of this material vary significantly between viruses, as well as the proteins that are needed for replication. After the infection, there is a period called the eclipse phase, when only few viruses are found in the infected cells. During this phase, the genome and all the viral machinery is exposed to the host, but the viral progeny is still small. Afterwards, there is a pause when virions accumulate inside or outside of the cell at an exponential rate. This pause is called the maturation phase. After some hours, lytic viruses cause cellular lysis with the cessation of all metabolic activity and the cells lose their structural integrity. Cells infected by non-lytic viruses can continue virion synthesis over a long period of time.

  The reproductive cycle of viruses may take hours or days. The infection of cells does not guarantee the production of viral progeny, which may be productive, restricted, aborted, or latent. A productive infection occurs in permissible cells and results in infectious viral particles. An abortive infection may occur in two circumstances: firstly, although the cell is sensitive to infection, it is not necessarily permissive, allowing the expression of only a few viral genes. The second circumstance is when a sensitive cell, permissive or not, is infected by defective viruses that do not have all the necessary viral genes for their replication. Furthermore, the cells can be temporarily permissible. In this case, the viral particles may remain in the cells until they become permissive or else some viral particles may be produced for a limited period of time by a fraction of the cell population. This type of infection is called restricted. In a latent infection, the viral genome persists in temporarily permissive cells without the destruction of the infected cells.

  Sign up to read

  Learn more about book
• 

  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.

  Sign up to read

  Learn more about book
• 

  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

  Sign up to read

  Learn more about book
• 

  eBook - PDF

  The Biology of Animal Viruses

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

    (Publisher)

  Even when the plasma membrane is de-stroyed by viruses, animal cells do not burst like bacteria, but rather shrink and leave an intact mass of debris that may enclose most of the viral progeny. The viral yield is equivalent to what bacterial virologists called the burst size. This can be measured in terms of the number of virus particles or of infectious units produced per cell. These two figures are not identical, for reasons dis-cussed in Chapter 2. THE ESSENTIAL STEPS IN MULTIPLICATION It is possible to dissect the viral multiplication cycle into several more or less sequential steps (although one process grades into the next, and after the first few hours several of the processes which follow are going on simultaneously): (a) attachment; (b) penetration, leading to or coincidental with (c) uncoating. This leads to (d) eclipse, the disappearance of infectious virions, during which 178 5. The Multiplication of DNA Viruses a complex series of biosynthetic events occurs, viz., (e) transcription of mRNA from specific sequences of the parental viral DNA, (f) translation of this mRNA into virus-coded enzymes and other early proteins, (g) replication of the viral DNA, (h) transcription of further mRNA from progeny as well as parental DNA, and (i) translation of these late mRNA's into structural and other virus-coded proteins some of which are involved in regulatory functions. Finally the eclipse phase ends with (j) assembly and release of new virions. Attachment Attachment of virions to the plasma membrane is electrostatic and follows the establishment of contact by collision between virions and cells. It is inde-pendent of temperature except in so far as this affects Brownian movement of virions and cells and thus the likelihood of their collision. Attachment will occur only if there is a certain affinity between the cell sur-face and the virions, areas of the cell membrane showing this affinity being called viral receptors.

  Sign up to read

  Learn more about book
• 

  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.
Passage contains an image

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