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The genus is distinguished on the basis of genetic characters.
Crystal structures of many enteroviruses have been resolved (Enterovirus A: coxsackievirus A7, coxsackievirus-A16, enterovirus A71; Enterovirus B: coxsackievirus A9, coxsackievirus B3, echovirus 1, echovirus 7, echovirus 11, echovirus 12, swine vesicular disease virus 1; Enterovirus C: poliovirus 1, poliovirus 2, poliovirus 3, coxsackievirus A21, coxsackievirus A24; Enterovirus D: enterovirus D68; Enterovirus E: enterovirus E1; Rhinovirus A: rhinovirus A1, rhinovirus A2, rhinovirus A16; Rhinovirus B: rhinovirus B14; Rhinovirus C: rhinovirus C15). CPs 1B, 1C and 1D of the human enteroviruses and rhinoviruses are among the largest in the family (VP1-3 chain lengths, 238–302 aa), and this is reflected in the typically long inter-β-strand loops, the larger than average thickness of the capsid wall (46 Å), and a surface relief that is strongly pronounced compared to most other picornaviruses. Encircling a raised area at the 5-fold axis is a 25 Å deep groove, or "canyon", into which the cellular receptor for poliovirus binds. The binding site for the pocket factor lies beneath the floor of this canyon within the 1D β-barrel. Virions can be converted by a variety of treatments (gentle heating, binding to receptor, or some neutralizing antibodies) to altered ('A') particles of 135S which lack 1A (VP4) and possess altered antigenicity.
Acid stability is variable. The virions of most enteroviruses are stable at pH 3.0, while those of rhinoviruses are unstable below pH 5–6. Similarly, the buoyant density in CsCl of the enterovirus virions is 1.30–1.34 g cm-3, while that of rhinoviruses ranges from 1.38 to 1.42 g cm-3. Sometimes a small proportion (about 1% of the population) of heavy particles (density: 1.43 g cm-3) can be observed for enteroviruses. Empty capsids are often observed in virus preparations.
Genome (Kitamura et al., 1981, Racaniello and Baltimore 1981, van der Werf et al., 1981): c. 7,100–7,450 nt (5′-UTR: 610–822 nt; ORF: 6,417–6,645 nt; 3′-UTR: 37–99 nt). The genome contains a type I IRES and no poly(C) tract. The cre is located in 2C (members of Enterovirus A, Enterovirus B, Enterovirus C and Enterovirus D) or 2A (members of Rhinovirus A) or 1D (members of Rhinovirus B) or 1B (members of Enterovirus C). Sequence identities for different enteroviruses, or between enteroviruses and rhinoviruses are more than 50% over the genome as a whole although it may be greater or less than this for particular genomic regions. The 5′-UTR of human rhinoviruses is shorter (ca. 650 nt) than that of enteroviruses, due to a deletion of approximately 100 nt between the IRES and the translation start site. Some members of Enterovirus C and Enterovirus D also have smaller deletions in this region. Members of Enterovirus E and Enterovirus F have a non-perfect duplication of the first ~100 nucleotides allowing the formation of a second clover-leaf-like RNA structure. Members of Enterovirus G have an insertion of about 30 nt approximately 65 nt from the 5′-end of the genome resulting in a longer stem-loop D in the cloverleaf structure. Varying size deletions in the same region have been observed in some of the human enteroviruses.
The deduced polyprotein of enteroviruses ranges from 2,138–2,214 amino acids. Genomes encode no L protein. 2A protein has proteinase activity with an active site cysteine residue (2Apro), which is related to the family of small bacterial serine proteases, cleaves the polyprotein at its own N-terminus. Members of Enterovirus K have a second 2Apro with an active site serine residue. Various strains of Enterovirus G have a porcine torovirus-like cysteine protease-encoding region inserted between the 2C and 3A gene regions. Certain hydrophobic molecules that bind to the capsid in competition with pocket factor exert a powerful antiviral action by interfering with receptor binding and/or uncoating. Antiviral, pocket-binding drugs have been described.
Viruses multiply primarily in the gastrointestinal tract or the upper respiratory tract or sometimes both, but they can also multiply in other tissues, e.g., nerve, muscle, etc. Infection may frequently be asymptomatic. Clinical manifestations include common cold, mild meningitis, encephalitis, myelitis, myocarditis and conjunctivitis. Swine vesicular disease virus is a variant of coxsackievirus B5 and causes a vesicular disease in pigs clinically indistinguishable from foot-and-mouth disease (genus Aphthovirus) and vesicular disease in pigs caused by Seneca Valley virus (genus Senecavirus). Cap-dependent translation of host mRNA is inhibited by 2Apro, which cleaves the host eukaryotic initiation factor 4G (eIF-4G). Many different cell surface molecules, many of them uncharacterized, serve as viral receptors. Well characterized receptor/virus interactions include poliovirus receptor (PVR) / polioviruses, coxsackievirus-adenovirus receptor (CAR) / coxsackie B viruses, inter-cellular adhesion molecule 1 (ICAM-l) / “major-group” rhinoviruses and some members of the Enterovirus C species, low-density lipoprotein receptor (LDLR) / “minor-group” rhinoviruses, decay-accelerating factor (DAF) / various enteroviruses, integrin VLA-2 / echovirus 1, and sialic acid / enterovirus D70. Poliovirus type 2, a member of the species Enterovirus C, is believed to have been eradicated through human intervention from circulation in human populations.
Approximately 75 enterovirus serotypes and 100 rhinovirus serotypes have been classified by means of neutralization of infectivity.
Entero-: from Greek enteron, 'intestine'
Members of a species of the genus Enterovirus:
The divergence (number of differences per site between sequences) between members of different Enterovirus species ranges from 0.29–0.59 for P1 and 0.1–0.48 for 3CD.
More than 300 virus types have been characterized genetically by phylogenetic clustering (Oberste et al., 1999, Palmenberg et al., 2009, Simmonds et al., 2010, McIntyre et al., 2013). Enterovirus A: 25 types, Enterovirus B: 63 types, Enterovirus C: 23 types, Enterovirus D: 5 types, Enterovirus E: 5 types, Enterovirus F: 7 types, Enterovirus G: 22 types, Enterovirus H: 1 type, Enterovirus I: 1 type, Enterovirus J: 6 types, Enterovirus K: 2 types, Enterovirus L: 1 type, Rhinovirus A: 80 types, Rhinovirus B: 32 types, Rhinovirus C: 57 types.
Certain viruses initially reported as novel echoviruses were later shown to have been misidentified. Thus echovirus 8 is the same serotype as echovirus 1, echovirus 10 is now reovirus 1, echovirus 28 is now human rhinovirus A1A, echovirus 22 is now human parechovirus 1, echovirus 23 is now human parechovirus 2. Similarly, coxsackievirus A23 is the same serotype as echovirus 9, and coxsackievirus A15 is the same serotype as coxsackievirus A11 and coxsackievirus A18 is the same serotype as coxsackievirus A13. Hepatitis A virus (genus Hepatovirus) was previously assigned the name enterovirus 72. Human rhinovirus 87 has been found to be a strain of enterovirus D68. A number of simian viruses (SV), previously listed as tentative members of the genus, have been moved to the genus Sapelovirus, species Sapelovirus B and renamed simian sapelovirus (SSV) 1 (formerly SV2), SSV-2 (formerly SV 49) and SSV-3 (formerly SV16, SV-18, SV42, SV44 and SV45). Simian agent 4 (SA4), SV4, SV28 and A2-plaque virus have been assigned to the species Enterovirus H. Simian enteroviruses N125 and N203 have been placed into a new type, enterovirus 108, which has been assigned to the species Enterovirus J, along with enterovirus 103 and simian virus 6. Type SV-47 remains unassigned to a species. Porcine enteroviruses (PEV) belonging to CPE group I (types 1-7 and 11-13) have been moved to the genus Teschovirus, species Teschovirus A, and renamed porcine teschovirus (PTV) 1-10. Members of the defunct species Porcine enterovirus A (PEV type 8; CPE group II) have been moved to the genus Sapelovirus and renamed Sapelovirus A (serotype porcine sapelovirus 1). The defunct species Porcine enterovirus B (PEV types 9, 10; CPE group III) has been renamed Enterovirus G.
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