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Viruses: Definition, Structure, Classification

  • Susanne ModrowEmail author
  • Dietrich Falke
  • Uwe Truyen
  • Hermann Schätzl
Reference work entry
  • 9.3k Downloads

Abstract

Viruses are infectious units with diameters of about 16 nm (circoviruses) to over 300 nm (poxviruses; Table 2.1). Their small size makes them ultrafilterable, i.e. they are not retained by bacteria-proof filters. Viruses have evolved over millions of years, and have adapted to specific organisms or their cells. The infectious virus particles, or virions, are composed of proteins and are surrounded in some species of viruses by a lipid membrane, which is referred to as an envelope; the particles contain only one kind of nucleic acid, either DNA or RNA. Viruses do not reproduce by division, such as bacteria, yeasts or other cells, but they replicate in the living cells that they infect. In them, they develop their genomic activity and produce the components from which they are made. They encode neither their own protein synthesis machinery (ribosomes) nor energy-generating metabolic pathways. Therefore, viruses are intracellular parasites. They are able to re-route and modify the course of cellular processes for the optimal execution of their own reproduction. Besides the genetic information encoding their structural components, they additionally possess genes that code for several regulatory active proteins (such as transactivators) and enzymes (e.g. proteases and polymerases).

Keywords

Prion Disease Bovine Spongiform Encephalopathy Infectious Virus Particle Human Prion Disease Protein Synthesis Machinery 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

2.1 What is a Virus?

Viruses are infectious units with diameters of about 16 nm (circoviruses) to over 300 nm (poxviruses; Table 2.1). Their small size makes them ultrafilterable, i.e. they are not retained by bacteria-proof filters. Viruses have evolved over longtime period, and have adapted to specific organisms or their cells. The infectious virus particles, or virions, are composed of proteins and are surrounded in some species of viruses by a lipid membrane, which is referred to as an envelope; the particles contain only one kind of nucleic acid, either DNA or RNA. Viruses do not reproduce by division, such as bacteria, yeasts or other cells, but they replicate in the living cells that they infect. In them, they develop their genomic activity and produce the components from which they are made. They encode neither their own protein synthesis machinery (ribosomes) nor energy-generating metabolic pathways. Therefore, viruses are intracellular parasites. They are able to re-route and modify the course of cellular processes for the optimal execution of their own reproduction. Besides the genetic information encoding their structural components, they additionally possess genes that code for several regulatory active proteins (such as transactivators) and enzymes (e.g. proteases and polymerases).
Table 2.1

Molecular biological characteristics of the different virus families, including some typical prototypes

Virus family

Subfamily/genus

Example

Envelope

Particle size/shape of the capsid or nucleocapsid

Genome: kind and size

Picornaviridae ( Sect. 14.1)

Enterovirus

Poliovirus, coxsackievirus, human enteroviruses, human rhinoviruses

No

28–30 nm/icosahedron

ssRNA; linear; positive strand; 7,200–8,400 nucleotides

Cardiovirus

Encephalomyocarditis virus, mengovirus, theilovirus

Aphthovirus

Foot-and-mouth disease virus

Parechovirus

Human parechovirus

Hepatovirus

Hepatitis A virus

Erbovirus

Equine rhinitis B virus

Kobuvirus

Aichi virus

Teschovirus

Porcine teschoviruses

Astroviridae ( Sect. 14.2)

Mamastrovirus

Human, bovine and feline astroviruses

No

27–30 nm/icosahedron

ssRNA; linear; positive strand; 6,800–7,900 nucleotides

Avastrovirus

Avian astroviruses

Caliciviridae ( Sect. 14.3)

Norovirus

Norwalk virus

No

27–34 nm/icosahedron

ssRNA; linear; positive strand; 7,500–8,000 nucleotides

Sapovirus

Sapporo virus

Vesivirus

Feline calicivirus

Lagovirus

Rabbit haemorrhagic disease virus

Nebovirus

Newbury-1 virus

Hepeviridae ( Sect. 14.4)

Hepevirus

Hepatitis E virus

No

27–34 nm/icosahedron

ssRNA; linear; positive strand; 7,200 nucleotides

Flaviviridae ( Sect. 14.5)

Flavivirus

Yellow fever virus, dengue virus, West Nile virus, tick-borne encephalitis virus

Yes

40–50 nm/icosahedron

ssRNA; linear; positive strand; 10,000 nucleotides

Pestivirus

Classical swine fever virus, bovine viral diarrhoea virus

Hepacivirus

Hepatitis C virus

Togaviridae ( Sect. 14.6)

Alphavirus

Sindbis virus, Semliki Forest virus, equine encephalitis viruses

Yes

60–70 nm/icosahedron

ssRNA; linear; positive strand; 12,000 nucleotides

Rubivirus

Rubella virus

Arteriviridae ( Sect. 14.7)

Arterivirus

Equine arteritis virus, porcine reproductive and respiratory syndrome virus

Yes

40–60 nm/icosahedron

ssRNA; linear; positive strand; 12,000–16,000 nucleotides

Coronaviridae ( Sect. 14.8)

Coronavirinae/Alphacoronavirus

Human coronaviruses 229E and NL63, feline coronavirus, porcine transmissible gastroenteritis virus

Yes

120–160 nm/helix

ssRNA; linear; positive strand; 25,000–35,000 nucleotides

Coronavirinae/Betacoronavirus

SARS-associated coronavirus, mouse hepatitis virus, bat corinaviruses HKU5 and HKU9

Coronavirinae/Gammacoronavirus

Avian infectious bronchitis virus

Torovirinae/Torovirus

Bovine and equine toroviruses

Rhabdoviridae ( Sect. 15.1)

Vesiculovirus

Vesicular stomatitis virus

Yes

65–180 nm/helix

ssRNA; linear; negative strand; 12,000 nucleotides

Lyssavirus

Rabies virus

Ephemerovirus

Bovine ephemeral fever virus

Novirhabdovirus

Infectious haematopoietic necrosis virus, viral haemorrhagic septicaemia virus

Bornaviridae ( Sect. 15.2)

Bornavirus

Borna disease virus

Yes

90 nm/helix

ssRNA; linear; negative strand; 9,000 nucleotides

Paramyxoviridae ( Sect. 15.3)

Respirovirus

Parainfluenza virus

Yes

150–250 nm/helix

ssRNA; linear; negative strand; 16,000–20,000 nucleotides

Rubulavirus

Mumps virus

Avulavirus

Newcastle disease virus

Morbillivirus

Measles virus, canine distemper virus, rinderpest virus

Henipavirus

Hendra virus, Nipah virus

Pneumovirus

Respiratory syncytial virus

Metapneumovirus

Human metapneumovirus

Filoviridae ( Sect. 15.4)

Marburgvirus

Marburg marburgvirus

Yes

80–700 nm/helix

ssRNA; linear; negative strand; 19,000 nucleotides

Ebolavirus

Zaire ebolavirus, Reston ebolavirus

Arenaviridae ( Sect. 16.1)

Arenavirus

Lymphocytic choriomeningitis virus, Lassa virus, Junín virus

Yes

50–300 nm/helix

ssRNA; linear; 2 segments; ambisense strands; 10,000–12,000 nucleotides

Bunyaviridae ( Sect. 16.2)

Orthobunyavirus

California encephalitis virus

Yes

100–120 nm/helix

ssRNA; linear; 3 segments; negative strand (ambisense in phleboviruses); 12,000 nucleotides

Phlebovirus

Rift Valley fever virus, sandfly fever virus

Nairovirus

Crimean-Congo fever virus, Nairobi sheep disease virus

Hantavirus

Hantaan virus, Puumala virus, Sin Nombre virus

Topsovirus

Tomato spotted wilt virus

Orthomyxoviridae ( Sect. 16.3)

Influenza A virus

Influenza A virus

Yes

120 nm/helix

ssRNA; linear; 7 or 8 segments; negative strand; 13,000–14,000 nucleotides

Influenza B virus

Influenza B virus

Influenza C virus

Influenza C virus

Thogotovirus

Thogoto virus, Dhori virus

Isavirus

Infectious salmon anaemia virus

Birnaviridae ( Sect. 17.1)

Avibirnavirus

Gumboro virus

No

60 nm/icosahedron

dsRNA; linear; 2 segments; 5,800–6,400 base pairs

Aquabirnavirus

Infectious pancreatic necrosis virus

Entomobirnavirus

Drosophila X virus

Reoviridae ( Sect. 17.2)

Orthoreovirus

Reoviruses

No

70–80 nm/icosahedron

dsRNA; linear; 10/11/12 segments; 18,000–19,000 base pairs

Orbivirus

Bluetongue virus, African horse sickness virus

Rotavirus

Rotaviruses

Coltivirus

Colorado tick fever virus

Aquareovirus

Golden shiner virus

Retroviridae ( Sect. 18.1)

Alpharetrovirus

Rous sarcoma virus

Yes

100 nm/icosahedron or cone

ssRNA; linear; positive strand, transcription into dsDNA; integration; 7,000–12,000 nucleotides

Betaretrovirus

Mouse mammary tumour virus

Jaagsiekte sheep retrovirus (ovine pulmonary adenomatosis virus)

Gammaretrovirus

Feline leukaemia virus, murine leukaemia virus

Deltaretrovirus

Human T-lymphotropic viruses 1 and 2, bovine leukaemia virus

Epsilonretrovirus

Diverse fish retroviruses

Lentivirus

Human immunodeficiency viruses

Spumavirus

Simian foamy virus

Hepadnaviridae ( Sect. 19.1)

Orthohepadnavirus

Hepatitis B virus

Yes

42 nm

DNA; partially double stranded; circular; 3,000–3,300 base pairs

Avihepadnavirus

Duck hepatitis B virus

Deltavirus (virusoid); infection along with hepatitis B virus as helper virus

Hepatitis D virus

Yes, composition to similar the envelope of hepatitis B viruses

ssRNA; circular; 1,900 nucleotides

Polyomaviridae ( Sect. 19.2)

Polyomavirus

BK polyomavirus, JC polyomavirus, simian virus 40

No

45 nm/icosahedron

dsDNA; circular; 5,000 nucleotides

Papillomaviridae ( Sect. 19.3)

Alphapapillomavirus

Human papillomaviruses 6, 10, 16, 18 and 32 (mucosa, oral/genital)

No

55 nm/icosahedron

dsDNA; circular; 8,000 nucleotides

Betapapillomavirus

Human papillomaviruses, 5, 9 and 49 (dermal)

Gammapapillomavirus

Human papillomaviruses 4, 48 and 50 (dermal)

Deltaapillomavirus

Ruminant papillomaviruses (cattle, sheep, deer)

Lambdapapillomavirus

Canine and feline papillomaviruses

Adenoviridae ( Sect. 19.4)

Mastadenovirus

Human and canine adenoviruses

No

70–80 nm/icosahedron

dsDNA; linear; 36,000–38,000 base pairs

Aviadenovirus

Avian adenoviruses

Siadenovirus

Turkey haemorrhagic enteritis virus

Atadenovirus

Chicken egg drop syndrome virus

Herpesviridae ( Sect. 19.5)

Alphaherpesvirinae

Herpes simplex viruses, varicella-zoster virus, bovine, equine, porcine, canine, feline and gallid herpesviruses

Yes

250–300 nm/icosahedron

dsDNA; linear; 150,000–250,000 base pairs

Betaherpesvirinae

Cytomegalovirus, human herpesvirus 6

Gammaherpesvirnae

Epstein-Barr virus, human herpesvirus 8, alcelaphine herpesvirus 1 (bovine malignant catarrhal fever virus)

Poxviridae ( Sect. 19.6)

Orthopoxvirus

Variola viruses, vaccinia virus, bovine and simian variola viruses

Yes

350–450 nm/complex

dsDNA; linear; 130,000–350,000 base pairs

Parapoxvirus

Orf virus

Avipoxvirus

Canarypox virus

Molluscipoxvirus

Molluscum contagiosum virus

Suipoxvirus

Swinepox virus

Yatapoxvirus

Tanapox virus, Yaba monkey tumour virus

Asfarviridae ( Sect. 19.7)

Asfivirus

African swine fever virus

Yes

200 nm/complex

dsDNA; linear; 180,000 base pairs

Parvoviridae ( Sect. 20.1)

Parvovirus

Feline panleucopenia virus, canine parvovirus, porcine parvovirus

No

20–25 nm/icosahedron

ssDNA; linear; 5,000 nucleotides

Erythrovirus

Parvovirus B19

Bocavirus

Human bocavirus, bovine bocavirus, canine minute virus

Amdovirus

Aleutian mink disease virus

Dependovirus

Adeno-associated viruses

Circoviridae ( Sect. 20.2)

Gyrovirus

Chicken anaemia virus

No

16–24 nm/icosahedron

ssDNA; circular; 1,700–2,000 nucleotides

Circovirus

Porcine circovirus, beak and feather disease virus

Anelloviridae ( Sect. 20.2)

Alphatorquevirus

Torque teno virus

Betatorquevirus

Torque teno mini virus

Gammatorquevirus

Torque teno midi virus

ssDNA single-stranded DNA, dsDNA double-stranded DNA, ssRNA single-stranded RNA, dsRNA double-stranded RNA

Viruses exist in different conditions. They can actively replicate in cells, and produce a great number of progeny viruses. This is known as a replicationally active state. After infection, some virus types can transition into a state of latency by integrating their genetic information into the genome of the host cell, or maintain it as an episome in an extrachromosomal status within infected cells. Certain viral genes can be transcribed during that time, contributing to the maintenance of latency (herpesviruses). In other cases, the expression of the viral genome is completely repressed over long periods of time (e.g. in some animal pathogenic retroviruses). In both cases, cellular processes or external influences can reactivate the latent genomes, leading to a new generation of infectious viruses. Depending on the virus type, the infection can have different consequences for the host cell:
  1. 1.

    It is destroyed and dies.

     
  2. 2.

    It survives, but continuously produces small numbers of viruses and is chronically (persistently) infected.

     
  3. 3.

    It survives and the viral genome remains in a latent state without producing infectious particles.

     
  4. 4.

    It is immortalized, thus gaining the capability of unlimited cell division, a process that can be associated with malignant transformation into a tumour cell.

     

2.2 How are Viruses Structured, and what Distinguishes them from Virusoids, Viroids and Prions?

2.2.1 Viruses

Infectious virus particles – also referred to as virions – are constituted of various basic elements (Fig. 2.1): inside, they contain an RNA genome or a DNA genome. Depending on the virus type, the nucleic acid is single-stranded or double-stranded, linear, circular or segmented. Single-stranded RNA and DNA genomes can have different polarity, and in certain cases the RNA genome is similar to messenger RNA, e.g. in picornaviruses and flaviviruses. A single-stranded genome that has the same polarity as the messenger RNA is referred to as a positive or plus strand. The genome forms a nucleocapsid complex with cellular histones (polyomaviruses) or viral proteins (e.g. rhabdoviruses, paraviruses, orthomyxoviruses, adenoviruses and herpesviruses). This nucleic acid-protein complex can be surrounded by particular protein structures, the capsids (in polyomaviruses, papillomaviruses, adenoviruses and herpesviruses). In some cases (such as picornaviruses, flaviviruses, togaviruses and parvoviruses), the nucleic acid interacts directly with the capsids. In viruses containing an envelope, the capsid layer can be absent (as in coronaviruses, rhabdoviruses, paramyxoviruses, orthomyxoviruses, bunyaviruses and arenaviruses).
Fig. 2.1

Structure of an enveloped viral capsid

Capsids are rod-shaped or cubic-spherical protein structures. In some virus types, they consist of multimeric units of only one polypeptide, in other cases they are composed of heteromeric complexes. The capsid protein subunits can aggregate into discrete subunits or even into so-called capsomeres, i.e. morphologically distinct structural components. Rod-shaped capsids have a helical symmetry. The two planes of symmetry, i.e. the longitudinal and the transversal axes, differ in length (Fig. 2.2a). By contrast, spherical capsids have an icosahedral structure with a rotational symmetry; an icosahedron consists of 20 equilateral triangles and 12 vertices (Fig. 2.2b). The symmetry axes have the same length: the fivefold symmetry axis is located at the vertices of the icosahedron; the threefold axis passes through the centre of a triangle, the twofold axis passes along the edges. The number of subunits of an icosahedron can be calculated by the formula \( 10{{\left( {n-1} \right)}^2}+2 \), where n indicates the number of morphologically distinguishable structures on the face of a triangle.
Fig. 2.2

Symmetry forms of viral capsids. (a) Helical symmetry; the symmetry planes run parallel to the longitudinal or transverse axis of the particle (e.g. tobacco mosaic virus capsid, nucleocapsid of paraviruses or orthomyxoviruses). (b) Cubic-spherical symmetry; icosahedron with rotational symmetry whose centres of the symmetry axes are at the vertices of the icosahedron (fivefold symmetry axis) in the middle of the triangle (threefold symmetry axis) and along the edges (twofold symmetry axis). Picornaviruses, parvoviruses and adenoviruses are examples of viruses with such capsid forms

The three-dimensional structures of the particles of a number of viruses have been resolved by X-ray structural analyses. Prerequisite is knowledge of the basic composition of the virus, i.e. information on which proteins form the capsid or the virus, as well as the nature of the viral genetic information and the sequence of the structural proteins. In addition, purification of virus particles must be possible and these must be available as a stable highly concentrated virus suspension on the order of several milligrams per millilitre. Finally, the purified virions or, alternatively, viral capsids, which are produced in cell culture or by genetic engineering, must be able to crystallize.

In some virus types, the capsids are surrounded by a lipid bilayer envelope, which is derived from cellular membrane systems. Viral and cellular proteins are embedded in the envelope, and are frequently modified into glycoproteins by sugar groups. Usually, viral surface components are clearly exposed, and they can protrude up to 20 nm from the particle surface. If such a membrane envelope is present, it renders the virus sensitive to inactivation by solvents and detergents. A tegument layer can be situated between the membrane and the capsid (herpesviruses), and contains additional viral protein components.

The exposed proteins and protein domains on the surface of the virus – either in the envelope or in the capsid – are subject to selection pressure by the immune system. Therefore, viruses change by mutation and selection preferentially the amino acid sequences of antibody-binding regions or epitopes, which are responsible for binding neutralizing immunoglobulins. In some species of viruses, this variability of the surface regions leads to the formation new subtypes. In addition to this continuous change of the surface of exposed regions that is determined by mutation and selection, in some virus types another source of variability is possible by genetic recombination, by which even large nucleic acid regions can be exchanged between different viruses. This can lead to substantial changes in the viruses involved and to the generation of new viral species.

2.2.2 Virusoids (Satellite Viruses), Viroids, Mimiviruses and Virophages

Satellite viruses, or virusoids, are small RNA or DNA molecules that code for one or two proteins with which they are associated. Their replication and spread is dependent on the presence of another virus. Virusoids are usually found together with plant viruses, but also hepatitis D virus, which can only proliferate when the cell is simultaneously infected with hepatitis B virus, is a virusoid ( Sect. 19.1.5). Viroids are plant pathogens and consist of a circular RNA (about 200–400 nucleotides) that does not code for proteins and exhibits a complex two-dimensional structure. A central sequence motif is highly conserved and essential for replication of these nucleic acid molecules. Other regions are variable and may be responsible for virulence. These infectious RNA molecules are replicated by cellular polymerases in a rolling circle mechanism ( Sect. 3.4), whereby secondary structures are formed at the transitions, which are known as a hammerhead because of their form. They have RNase activity, and autocatalytically cleave the concatemeric RNA strands that result after replication. Ribozymes, small RNA species with sequence-specific RNase activity ( Sect. 9.3), are derived from the hammerhead-like RNA structures.

Mimiviruses are a family of very large DNA viruses which were discovered by Didier Raoult in the amoeba Acanthamoeba polyphaga only in 2004. These viruses were originally regarded as bacteria because of the extraordinary size of their spherical capsids (400 nm) and protein filaments, which protrude extremely from the surface, conferring the virions with an apparent size of up to 800 nm. Therefore, they were denominated “mimiviruses” as an abbreviation for “mimicking viruses”. The DNA genome of mimiviruses comprises 1.2 million base pairs and encompasses more than 1,200 putative genes. Even larger mamaviruses have been discovered in amoebae, which can be infected by parasitic viruses. These significantly smaller viruses (sputnikvirus), also known as virophages, can multiply in amoebae only if they are concurrently infected by mamaviruses. However, sputniks do not use mamaviruses only as a helper virus, but also inhibit their proliferation and morphogenesis, thus making them virtually sick.

2.2.3 Prions

In animals and humans, prions always cause fatal neurodegenerative disorders. They can be transmitted within a species, and – albeit limited – to other organisms beyond species boundaries ( Chap. 21). The pathogen responsible (prion, from “proteinaceous infectious particle”) does not require a coding nucleic acid in the infectious agent. Prions are composed of the pathological isoform (PrPSc), which exists especially in β-sheet conformation, and of a non-pathological cellular prion protein (PrPC), which is present predominantly in α-helical conformation. The conversion of the PrPC α-helical conformation into the β-sheet PrPSc variant is associated with completely different biochemical properties, and is the key pathogenetic basic principle of prion diseases. After its synthesis, the cellular protein PrPC arrives in the cytoplasmic membrane. PrPC is active at the cell surface only for a limited time, and is subsequently degraded in the endosomes. During this process, a small proportion of PrPC proteins are constantly transformed into PrPSc variants. This process is referred to as prion conversion. PrPSc proteins cannot be efficiently degraded and accumulate in the cells. The function of PrPC has not been completely resolved. Experiments with knockout mice containing a deletion of the PrP coding genome sequences revealed that PrPC appears to be dispensable for development and survival of the mice. However, without PrPC they cannot develop a prion disease.

Human prion diseases include Creutzfeldt-Jakob disease, kuru and variant Creutzfeldt-Jakob disease. In animals, the most famous representatives are scrapie (sheep), bovine spongiform encephalopathy (cattle) and chronic wasting disease (deer). The peculiarity of prion diseases is that they appear in three manifestations: acquired infectious (exogenous), sporadic (endogenous) and genetic (endogenous). Inasmuch as prions are restricted to the central nervous system, their infectious transmission is generally limited.

2.3 What Criteria Determine the Classification System of Virus Families?

The taxonomic classification of viruses into different families is done by an international commission of virologists and is continuously adapted to current insights. It is based on the following main criteria:
  1. 1.

    The nature of the genome (RNA or DNA) and the form in which it is present, i.e. as a single or a double strand, in positive or negative sense, linear or circular, segmented or continuous; also the arrangement of genes on the nucleic acid is important for the definition of individual families.

     
  2. 2.

    The symmetry form of the capsids.

     
  3. 3.

    The presence of an envelope.

     
  4. 4.

    The size of the virion.

     
  5. 5.

    The site of viral replication within the cell (cytoplasm or nucleus).

     

The further subdivision into genera and virus types is largely based on serological criteria and the similarity of genome sequences. The different virus families and their important human and animal pathogenic prototypes are summarized in Table 2.1.

Further Reading

  1. Chiu W, Burnett RM, Garcea RL (1997) Structural biology of viruses. Oxford University Press, New YorkGoogle Scholar
  2. Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (2005) Virus taxonomy. VIIIth report of the international committee on taxonomy of viruses. Academic, San DiegoGoogle Scholar
  3. Fraenkel-Conrat H (1985) The viruses. Catalogue, characterization, and classification. Plenum, New YorkGoogle Scholar
  4. International Committee on Taxonomy of Viruses (2012) ICTV home. http://ictvonline.org/
  5. Knipe DN, Howley PM (eds) (2006) Fields virology, 5th edn. Lippincott-Raven, New YorkGoogle Scholar
  6. Nermuth MV, Steven AC (1987) Animal virus structure. Elsevier, AmsterdamGoogle Scholar
  7. Richman DD, Whitley RJ, Hayden FG (2002) Clinical virology, 2nd edn. ASM Press, Washington, DCGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2013

Authors and Affiliations

  • Susanne Modrow
    • 1
    Email author
  • Dietrich Falke
    • 2
  • Uwe Truyen
    • 3
  • Hermann Schätzl
    • 4
  1. 1.Inst. Medizinische, Mikrobiologie und HygieneUniversität RegensburgRegensburgGermany
  2. 2.MainzGermany
  3. 3.Veterinärmedizinische Fak., Inst. Tierhygiene undUniversität LeipzigLeipzigGermany
  4. 4.Helmholtz Zentrum München, Institut für VirologieTU MünchenMunichGermany

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