A Picornavirus is a virus
belonging to the family Picornaviridae.
Picornaviruses are non-enveloped, positive-stranded RNA viruses with an icosahedral capsid. The genome
RNA
is unusual because it has a protein on the 5' end that is used as a primer for transcription by RNA polymerase. The name is derived from pico
meaning small, and RNA referring to the ribonucleic acid genome, so "picornavirus" literally
means small RNA virus.
Picornaviruses
are separated into nine distinct genera and include many important pathogens of
humans and animals.[1] The diseases they cause are varied, ranging from
acute "common-cold"-like illnesses, to poliomyelitis, to chronic infections in livestock. Two main
categories are enteroviruses and rhinoviruses.
Classification
Picornaviruses
are classed under Baltimore's
viral classification system as group IV viruses as they contain a
single stranded, positive sense RNA genome
of between 7.2 and 9.0 kb in length. Like most positive sense RNA genomes, the
genetic material alone is infectious; although substantially less virulent than if contained within the viral particle, the RNA
can have increased infectivity when transfected into cells. The genome itself
is the same sense as mammalian mRNA, being read 5’ to 3’. Unlike mammalian mRNA Picornaviruses do not have a 5’ CAP but a
virally encoded protein known as VPg, however like mammalian mRNA the genome
does have a poly A tail at the 3’ end. There is an un-translated region (UTR)
at both ends of the Picornavirus genome. The 5’ UTR is longer, being around
600-1200 BP in length, compared to that of the 3’ UTR, which is around
50-100bp. It is thought that the 5’ UTR is important in translation and the 3’
in negative strand synthesis; however the 5’ end may also have a role to play
in virulence of the virus. The rest of the genome encodes structural proteins
at the 5’ end and non-structural proteins at the 3’ end in a single
polyprotein. Experimental data from single step growth-curve-like experiments
have allowed scientists to look at the replication of the picornaviruses in
great detail. The whole of replication occurs within the host cell cytoplasm
and infection can even happen in cells that do not contain a nucleus (known as enucleated cells) and those treated with actinomycin D (this antibiotic would inhibit viral replication
if this occurred in the nucleus.)
Picornaviruses
are separated into nine distinct genera. Contained within the picornavirus
family are many organisms of importance as vertebrate and human pathogens, shown in the table below.
Picornavirus
Genera, Species and Serotypes
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two
types: bovine enterovirus (BEV) 1 and BEV-2
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Human
enterovirus A
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21
types including some coxsackie A viruses and
enteroviruses
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Human
enterovirus B
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57
types including enteroviruses, coxsackie B viruses, echoviruses, and swine vesicular disease virus
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Human
enterovirus C
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14
types including some coxsackie A viruses and
enteroviruses
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Human
enterovirus D
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three
types: EV-68, EV-70, EV-94
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three
types: poliovirus (PV) 1, PV-2 and PV-3
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one
type: porcine enterovirus (PEV) 8
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Porcine
enterovirus B
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two
types: PEV-9 and PEV-10
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one
type: simian enterovirus (SEV) A1
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Human
rhinovirus A
*
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74
serotypes
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Human
rhinovirus B
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25
serotypes
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Human
rhinovirus C
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7
serotypes
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one
serotype: Hepatitis A virus (HAV)
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one
type: avian encephalomyelitis virus (AEV)
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one
serotype: encephalomyocarditis virus (EMCV). Note: Columbia SK
virus, Maus Elberfeld
virus and Mengovirus are strains of EMCV.
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five
types: Theiler's murine encephalomyellitis virus (TMEV), Vilyuisk human encephalomyelitis virus (VHEV), Theiler-like
virus (TLV) of rats, Saffold virus (SAFV) 1 and SAFV-2
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seven
serotypes: O, A, C, Southern African Territories (SAT) 1, SAT 2, SAT 3 and
Asia 1
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single
serotype: equine rhinitis A virus (ERAV)
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Human
parechovirus
*
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six
types: Human parechovirus (HPeV) 1, HPeV-2, HPeV-3, HPeV-4, HPeV-5, HPeV-6
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Possibly
three types have been described
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Equine
rhinitis B virus
*
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Three
types: equine rhinitis B virus (ERBV) 1, ERBV-2, ERBV-3
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single
serotype: Aichi virus (AiV)
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Single
serotype: bovine kobuvirus (BKV)
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11
serotypes: porcine teschovirus (PTV) 1 to PTV-11
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Sources
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Enteroviruses
infect the enteric tract as it is visible from its name. On the other
hand, rhinoviruses infect primarily the nose
and the throat. Enteroviruses replicate at 37°C, whereas Rhinoviruses
grow better at 33°C, as this is the lower temperature of the nose.
Enteroviruses are stable under acid conditions and thus they are able to
survive exposure to gastric acid. In contrast, Rhinoviruses
are acid-labile and that is the reason why Rhinoviruses are restricted to the
nose and throat.
The
plant picornaviruses have a number of properties that are distinct from the
animal viruses. They have been classified into a superfamily Secoviridae
containing the families Comoviridae (genera Comovirus, Fabavirus and Nepovirus), Sequiviridae (genera Sequivirus and Waikavirus) and a number
of unassigned genera (Cheravirus, Sadwavirus and Torradovirus (type
species Tomato torrado
virus)).[3]
The
capsid is an arrangement of 60 protomers in a tightly packed Icosahedral structure. Each protometer consists of 4 polypeptides known as VP (viral protein)1, 2, 3 and 4. VP2 and
VP4 polypeptides originate from one protomer known as VP0 that is cleaved to give the different capsid components. The Icosahedral is said to have a triangulation number of 3, this
means that in the icosahedral structure each of the 60
triangles that make up the capsid are split into 3 little triangles with a
subunit on the corner. Depending on the type and degree of dehydration the
viral particle is around 27-30 nm in diameter. The viral genome is around
2500 nm in length so we can therefore conclude that it must be tightly
packaged within the capsid along with substances such as sodium
ions in order to cancel out the negative charges on the RNA caused by the phosphate groups.
The
viral particle binds to cell surface receptors. This causes a conformational change
in the viral capsid proteins, and myristic acids are released. These acids form a pore in the
cell membrane through which RNA is injected[1].
Once inside the cell, the RNA un-coats and the (+) strand RNA genome is
replicated through a double-stranded RNA intermediate that is formed using
viral RDRP (RNA-Dependent RNA polymerase). Translation by host cell ribosomes
is not initiated by a 5' G cap as usual, but rather is initiated by an IRES
(Internal Ribosome Entry Site). The viral lifecycle is very rapid with the
whole process of replication being completed on average within 8 hours. However
as little as 30 minutes after initial infection, cell protein synthesis
declines to almost zero output – essentially the macromolecular synthesis of
cell proteins is “shut off”. Over the next 1–2 hours there is a loss of
margination of chromatin and homogeneity in the nucleus, before the viral proteins start to
be synthesized and a vacuole appears in the cytoplasm close to the nucleus that
gradually starts to spread as the time after infection reaches around 3 hours.
After this time the cell plasma membrane becomes permeable, at 4–6 hours the
virus particles assemble, and can sometimes be seen in the cytoplasm. At around
8 hours the cell is effectively dead and lyses to release the viral particles.
In
1897, foot-and-mouth disease
virus (FMDV), the first animal virus, was discovered. FMDV is the prototypic
member of the Aphthovirus genus in the Picornaviridae family. [2] The plaque assay was developed using
poliovirus. Both RNA dependent RNA polymerase and polyprotein synthesis were
discovered by studying poliovirus infected cells.
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