Virus Replication

Abstract

Viruses are obligate intracellular parasites, relying on their host cells to provide the basic machinery to allow them to replicate. Their basic structure is that of a nucleic acid–protein complex, often with an outer lipid envelope. The outer proteins of the virus both protect the viral genome (which may be deoxyribonucleic acid or, unlike cellular genomes, ribonucleic acid) and enable it to identify and infect suitable target cells. Movement between hosts is entirely passive, but once they encounter a suitable host cell viruses can begin a cycle that can produce hundreds of new viruses within a very short time. In a productive infection, recognition of external structures on the cell is followed by entry, alteration of cellular function to support a time‐dependent cycle of virus‐specific macromolecular synthesis, assembly of the next generation of virus particles, and release from the cell. However, while laboratory experiments focus on productive infections where the host cell is rapidly turned into a virus factory, many other types of infection exist, some of them allowing the virus to exist alongside its host for long periods of time.

Key Concepts:

  • The initial interaction between a virus and its host cell is mediated by proteins (often with attached sugars) on the surface of the virus and by proteins and other structures on the host cell. These allow the virus to select the nature of its target cell with great precision and at least to some extent to confirm its suitability before committing to infection.

  • The receptors used in the process of infection are highly varied. Individual viruses can use multiple receptors, or a series of receptors of increasing specificity.

  • Once bound to the host cell, viruses enter by a range of mechanisms, often involving uptake into vacuoles, although other routes such as fusion with the cell membrane may be used. Once within the cell, viruses move to specific sites where they can replicate.

  • Viruses can escape from vacuoles within the cell by diverting the cell's attempts to digest them.

  • Viruses replicate at various locations within the cell. Most DNA viruses infecting eukaryotic cells replicate in the nucleus (with the exception of the nucleocytoplasmic large DNA viruses) while most RNA viruses replicate in the cytoplasm (since the DNA replication machinery within the nucleus it usually of little use to them).

  • Viruses alter the cellular machinery to facilitate the production of the next generation of viruses, and repress cellular and immunological controls that attempt to prevent this.

  • Different viral genes are expressed at different stages of replication. Those expressed earlier on are often regulatory, or enzymes involved in the replication process. Genes expressed later are generally for the proteins that make up the virus particle (structural proteins) or those involved in viral assembly.

  • Seven basic replication strategies exist based on genome type (including DNA or RNA and single‐ or double‐stranded genomes) but these may vary widely within a specific type.

  • Simple DNA viruses can use (or induce the production of) the cellular DNA synthetic machinery, whereas more complex viruses carry genes for the enzymes they need, making the process of replication more efficient.

  • RNA viruses need to carry or produce their own polymerase to make RNA from an RNA template, since such enzymes are not present at useful levels in cells. Some RNA viruses do this by using their viral genome as an mRNA when they enter their host cell, whereas those that require transcription to produce mRNAs have to carry a suitable (and often rather large) polymerase within the virus particle.

  • Some viruses have genomes in multiple parts (segments) and must have ways to make sure that all of the necessary segments are packaged. Some plant viruses actually package each segment separately, relying on each target cell being infected multiple times.

  • Viruses that require a lipid envelope (enveloped viruses) can acquire this from a range of cellular sources, including the plasma membrane or internal membranes. Acquisition of lipid at the plasma membrane allows the virus to exit from the cell by budding.

  • Viruses without a lipid envelope are often released by active cell lysis or simply by the disintegration of a dying cell.

Keywords: virus; virology; replication; receptor; infection; DNA; RNA; assembly; latency

Figure 1.

Major cellular structures involved in virus replication. Figure reprinted with permission from Harper DR (2011) Viruses: Biology, Applications and Control. New York: Garland Science.

Figure 2.

A generalised scheme of a (productive) virus infection, from entry to release. Figure reprinted with permission from Harper DR (2011) Viruses: Biology, Applications and Control. New York: Garland Science.

Figure 3.

A general guide to viral replication strategies. Figure reprinted with permission from Harper DR (2011) Viruses: Biology, Applications and Control. New York: Garland Science.

Figure 4.

Binding and entry of human immunodeficiency virus (HIV) to a target cell. Figure reprinted with permission from Harper DR (2011) Viruses: Biology, Applications and Control. New York: Garland Science.

Figure 5.

A bacterial virus (bacteriophage) of the family Myoviridae, showing the contractile tail structure. Copyright AmpliPhi Biosciences.

Figure 6.

Budding of a member of the Retroviridae from the surface of an infected cell. Figure reprinted from Harper DR (2011) Viruses: Biology, Applications and Control. New York: Garland Science; images kindly provided by Dr. Ian Chrystie, St. Thomas's Hospital, London.

Figure 7.

Differing effects of virus infections. Figure reprinted from Harper DR (2011) Viruses: Biology, Applications and Control, with permission from Garland Science.

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Further Reading

Abedon ST and Calendar RL (2006) The Bacteriophages. Oxford: Oxford University Press.

Fields BN and Howley PM (2007) Virology, 5th edn. Philadelphia: Lipincott Williams & Wilkins.

Harper DR (2011) Viruses: Biology, Applications and Control. New York: Garland Science.

Hull R (2009) Comparative Plant Virology, 2nd edn. New York: Academic Press.

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How to Cite close
Harper, David R(May 2012) Virus Replication. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0000438.pub2]