Viruses: Definition, Structure, Classification

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


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).


Prion Disease Bovine Spongiform Encephalopathy Infectious Virus Particle Human Prion Disease Protein Synthesis Machinery 
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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




Particle size/shape of the capsid or nucleocapsid

Genome: kind and size

Picornaviridae ( Sect. 14.1)


Poliovirus, coxsackievirus, human enteroviruses, human rhinoviruses


28–30 nm/icosahedron

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


Encephalomyocarditis virus, mengovirus, theilovirus


Foot-and-mouth disease virus


Human parechovirus


Hepatitis A virus


Equine rhinitis B virus


Aichi virus


Porcine teschoviruses

Astroviridae ( Sect. 14.2)


Human, bovine and feline astroviruses


27–30 nm/icosahedron

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


Avian astroviruses

Caliciviridae ( Sect. 14.3)


Norwalk virus


27–34 nm/icosahedron

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


Sapporo virus


Feline calicivirus


Rabbit haemorrhagic disease virus


Newbury-1 virus

Hepeviridae ( Sect. 14.4)


Hepatitis E virus


27–34 nm/icosahedron

ssRNA; linear; positive strand; 7,200 nucleotides

Flaviviridae ( Sect. 14.5)


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


40–50 nm/icosahedron

ssRNA; linear; positive strand; 10,000 nucleotides


Classical swine fever virus, bovine viral diarrhoea virus


Hepatitis C virus

Togaviridae ( Sect. 14.6)


Sindbis virus, Semliki Forest virus, equine encephalitis viruses


60–70 nm/icosahedron

ssRNA; linear; positive strand; 12,000 nucleotides


Rubella virus

Arteriviridae ( Sect. 14.7)


Equine arteritis virus, porcine reproductive and respiratory syndrome virus


40–60 nm/icosahedron

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

Coronaviridae ( Sect. 14.8)


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


120–160 nm/helix

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


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


Avian infectious bronchitis virus


Bovine and equine toroviruses

Rhabdoviridae ( Sect. 15.1)


Vesicular stomatitis virus


65–180 nm/helix

ssRNA; linear; negative strand; 12,000 nucleotides


Rabies virus


Bovine ephemeral fever virus


Infectious haematopoietic necrosis virus, viral haemorrhagic septicaemia virus

Bornaviridae ( Sect. 15.2)


Borna disease virus


90 nm/helix

ssRNA; linear; negative strand; 9,000 nucleotides

Paramyxoviridae ( Sect. 15.3)


Parainfluenza virus


150–250 nm/helix

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


Mumps virus


Newcastle disease virus


Measles virus, canine distemper virus, rinderpest virus


Hendra virus, Nipah virus


Respiratory syncytial virus


Human metapneumovirus

Filoviridae ( Sect. 15.4)


Marburg marburgvirus


80–700 nm/helix

ssRNA; linear; negative strand; 19,000 nucleotides


Zaire ebolavirus, Reston ebolavirus

Arenaviridae ( Sect. 16.1)


Lymphocytic choriomeningitis virus, Lassa virus, Junín virus


50–300 nm/helix

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

Bunyaviridae ( Sect. 16.2)


California encephalitis virus


100–120 nm/helix

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


Rift Valley fever virus, sandfly fever virus


Crimean-Congo fever virus, Nairobi sheep disease virus


Hantaan virus, Puumala virus, Sin Nombre virus


Tomato spotted wilt virus

Orthomyxoviridae ( Sect. 16.3)

Influenza A virus

Influenza A virus


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


Thogoto virus, Dhori virus


Infectious salmon anaemia virus

Birnaviridae ( Sect. 17.1)


Gumboro virus


60 nm/icosahedron

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


Infectious pancreatic necrosis virus


Drosophila X virus

Reoviridae ( Sect. 17.2)




70–80 nm/icosahedron

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


Bluetongue virus, African horse sickness virus




Colorado tick fever virus


Golden shiner virus

Retroviridae ( Sect. 18.1)


Rous sarcoma virus


100 nm/icosahedron or cone

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


Mouse mammary tumour virus

Jaagsiekte sheep retrovirus (ovine pulmonary adenomatosis virus)


Feline leukaemia virus, murine leukaemia virus


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


Diverse fish retroviruses


Human immunodeficiency viruses


Simian foamy virus

Hepadnaviridae ( Sect. 19.1)


Hepatitis B virus


42 nm

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


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)


BK polyomavirus, JC polyomavirus, simian virus 40


45 nm/icosahedron

dsDNA; circular; 5,000 nucleotides

Papillomaviridae ( Sect. 19.3)


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


55 nm/icosahedron

dsDNA; circular; 8,000 nucleotides


Human papillomaviruses, 5, 9 and 49 (dermal)


Human papillomaviruses 4, 48 and 50 (dermal)


Ruminant papillomaviruses (cattle, sheep, deer)


Canine and feline papillomaviruses

Adenoviridae ( Sect. 19.4)


Human and canine adenoviruses


70–80 nm/icosahedron

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


Avian adenoviruses


Turkey haemorrhagic enteritis virus


Chicken egg drop syndrome virus

Herpesviridae ( Sect. 19.5)


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


250–300 nm/icosahedron

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


Cytomegalovirus, human herpesvirus 6


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

Poxviridae ( Sect. 19.6)


Variola viruses, vaccinia virus, bovine and simian variola viruses


350–450 nm/complex

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


Orf virus


Canarypox virus


Molluscum contagiosum virus


Swinepox virus


Tanapox virus, Yaba monkey tumour virus

Asfarviridae ( Sect. 19.7)


African swine fever virus


200 nm/complex

dsDNA; linear; 180,000 base pairs

Parvoviridae ( Sect. 20.1)


Feline panleucopenia virus, canine parvovirus, porcine parvovirus


20–25 nm/icosahedron

ssDNA; linear; 5,000 nucleotides


Parvovirus B19


Human bocavirus, bovine bocavirus, canine minute virus


Aleutian mink disease virus


Adeno-associated viruses

Circoviridae ( Sect. 20.2)


Chicken anaemia virus


16–24 nm/icosahedron

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


Porcine circovirus, beak and feather disease virus

Anelloviridae ( Sect. 20.2)


Torque teno virus


Torque teno mini virus


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.
  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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