Cricket paralysis virus | |
---|---|
Virus classification | |
(unranked): | Virus |
Realm: | Riboviria |
Kingdom: | Orthornavirae |
Phylum: | Pisuviricota |
Class: | Pisoniviricetes |
Order: | Picornavirales |
Family: | Dicistroviridae |
Genus: | Cripavirus |
Species: | Cricket paralysis virus |
Cricket paralysis virus (CrPV) is a paralytic disease affecting crickets. It was initially discovered in Australian field crickets ( Teleogryllus commodus and Teleogryllus oceanicus ) by Carl Reinganum and his colleagues at the Victorian Plant Research Institute (Burnley, Melbourne, Australia). The disease spread rapidly through a breeding colony as well as through a laboratory population causing about 95% mortality. This was the first recorded isolate of the virus [1] and is generally referred to as CrPVvic to distinguish it from subsequent isolates.[ citation needed ]
The spheroidal, non-enveloped virus particles of CrPV are about 27 nm diameter in negatively-stained electron micrographs and contain a single piece of positive-sense ssRNA. The virion is composed of four capsid proteins with molecular masses generally reported to be 33, 31 and 30 kilodaltons with a minor VP4 protein of about 8 kDa. The particles resemble those of the mammalian picornaviruses but CrPV virions sediment at a faster rate (167 S) than poliovirus particles (158 S) in sucrose rate-zonal gradients and, in isopycnic neutral cesium chloride gradients, CrPV particles are denser than those of poliovirus (1.368 g/cm3 vs 1.340 g/cm3 respectively). [2] [3] [4]
CrPV has been detected in a number of insect species from at least five different orders of the class Insecta, in both natural and laboratory populations, and is usually identified by standard serological methods. The infections include not only the Australian cricket species but the New Zealand cricket, Pteronemobius nigrovus , as well as the European house cricket, Acheta domesticus . [3] CrPV does not appear to infect locusts. It is a commonly detected virus in honeybees as an inapparent infection. [5]
The strain CrPVbrk was isolated from the cricket A. domesticusc. 1980, following a major population collapse at a cricket rearing farm in Georgia in the US. [3] A related virus from Arkansas, US, initially called Pseudoplusia includens virus and redesignated CrPVark, was recorded in the mid-1980s. [6] The brk and ark strains are closely related serologically but appear to be very distantly related to the other CrPV isolates so, despite their physical and chemical similarities, it remains speculative that these two American isolates are actually strains of CrPV. [7]
Reported detections and/or isolations of CrPV have been made in Australia, New Zealand, the United States, the United Kingdom and Indonesia. CrPV has one of the widest host-ranges of any virus, insect or not. [3] The potential for the use of CrPV as a biological control agent for insects has been suggested. In laboratory experiments CrPVbrk proved to be extremely infectious and pathogenic for adult Ceratitis capitata (Mediterranean fruit fly). [8] Detailed studies have also been made on the use of a CrPV strain to control the European olive fruit fly (Dacus oleae). [9]
In 2011, a "cricket paralysis virus" was reported to be involved in other catastrophic collapses in American cricket rearing facilities. A similar report from the UK and European cricket breeders, however, refers to a "cricket paralysis virus" but has identified the causative agent as a small DNA-containing virus, Acheta domesticus densovirus; [10] thus, the North American outbreaks are probably not due to the small RNA virus taxonomically referred to as CrPV. [11] [12] Over 60 million crickets died as a result of the outbreak. [13] Whatever the causative virus, switching to a different species for American breeders is more difficult than it is in Europe, as Acheta domesticus is currently the only cricket approved for commercial distribution, and any new proposals are scrutinized through a permitting process. [12]
CrPV has been shown to replicate in continuously cultured cell lines derived from the fruit fly Drosophila melanogaster and other insect cell lines. This ability enabled detailed studies on the replication strategy of the virus. The fact that a demonstrable cytopathic effect was also produced in these cultured cell infections led to the development of sensitive titration assay methods similar to those employed in studies of mammalian picornaviruses. In the 1990s large-scale production of the virus in cell suspension cultures of Drosophila or Trichoplusia ni cells made x-ray crystallographic studies feasible. CrPV was the first insect virus to have its crystal structure determined. [14]
Early studies conducted in the 1970s and 1980s showed the occurrence of post-translational processing of a large polyprotein produced during the course of infection of Drosophila cells with CrPV. This was reminiscent of the post-translational cleavages occurring when mammalian cells are infected with vertebrate picornaviruses such as poliovirus. However, the relative amounts of the resultant proteins resulting from the cleavages were puzzlingly unequal with CrPV in contrast to the equimolar levels produced by picornaviruses. Thus, despite some of the physical and genomic translation similarities that CrPV shared with mammalian picornaviruses, classifying CrPV as an insect "picornavirus" was justifiably contentious.[ citation needed ]
In the later 1990s the elucidation of the crystal structure of CrPV showed that while the conformation of its capsid proteins closely resembled those of picornaviruses, detailed analysis of the complete CrPV genome exposed critical differences. Picornavirus genomes contain only a single open reading frame (ORF) which is translated into a single polyprotein, but CrPV, as well as several other related insect viruses, is translated from two ORFs each driven by a respective internal ribosome entry site (IRES). Also the capsid proteins are encoded at the 3' end of the CrPV genome, the opposite of that for picornaviruses as well being differently ordered within the genome. These crucial characteristics led to the formation of the family Dicistroviridae by the International Committee on Taxonomy of Viruses (ICTV). CrPV is in the genus Cripavirus within this family. [2] [11] [14] [15]
Poliovirus, the causative agent of polio, is a serotype of the species Enterovirus C, in the family of Picornaviridae. There are three poliovirus serotypes, numbered 1, 2, and 3.
Picornaviruses are a group of related nonenveloped RNA viruses which infect vertebrates including fish, mammals, and birds. They are viruses that represent a large family of small, positive-sense, single-stranded RNA viruses with a 30 nm icosahedral capsid. The viruses in this family can cause a range of diseases including the common cold, poliomyelitis, meningitis, hepatitis, and paralysis.
Foot-and-mouth disease virus (FMDV) is a virus in the genus Aphthovirus that causes foot-and-mouth disease. As a member of the family Picornaviridae, FMDV is a positive-sense, single-stranded RNA virus. Like other members of the Picornavirus family, FMDV is small and unenveloped, with an icosahedral capsid.
Enterovirus is a genus of positive-sense single-stranded RNA viruses associated with several human and mammalian diseases. Enteroviruses are named by their transmission-route through the intestine.
Dicistroviridae is a family of viruses in the order Picornavirales. Invertebrates, including aphids, leafhoppers, flies, bees, ants, and silkworms, serve as natural hosts. There are 15 species in this family, assigned to three genera. Diseases associated with this family include: DCV: increased reproductive potential. extremely pathogenic when injected with high associated mortality. CrPV: paralysis and death.
An internal ribosome entry site, abbreviated IRES, is an RNA element that allows for translation initiation in a cap-independent manner, as part of the greater process of protein synthesis. Initiation of eukaryotic translation nearly always occurs at and is dependent on the 5' cap of mRNA molecules, where the translation initiation complex forms and ribosomes engage the mRNA. IRES elements, however allow ribosomes to engage the mRNA and begin translation independently of the 5' cap.
Acheta domesticus, commonly called the house cricket, is a species of cricket most likely native to Southwestern Asia, but between 1950 and 2000 it became the standard feeder insect for the pet and research industries and spread worldwide. They can be kept as pets themselves, as this has been the case in China and Japan.
Orthoreovirus is a genus of viruses, in the family Reoviridae, in the subfamily Spinareovirinae. Vertebrates serve as natural hosts. There are ten species in this genus. Diseases associated with this genus include mild upper respiratory tract disease, gastroenteritis, and biliary atresia. Mammalian orthoreovirus 3 induces cell death preferentially in transformed cells and therefore displays inherent oncolytic properties.
Parechovirus B, formerly called the Ljungan virus, was first discovered in the mid-1990s after being isolated from a bank vole near the Ljungan river in Medelpad county, Sweden. It has since been established that Parechovirus B, which is also found in several places in Europe and America, causes serious illness in wild as well as laboratory animals. Several scientific articles have recently reported findings indicating that Parechovirus B is associated with malformations, intrauterine fetal death, and sudden infant death syndrome in humans. In addition, studies are being conducted worldwide to investigate the possible connection of the virus to diabetes, neurological and other illnesses in humans.
Pleconaril (Picovir) is an antiviral drug that was being developed by Schering-Plough for prevention of asthma exacerbations and common cold symptoms in patients exposed to picornavirus respiratory infections. Pleconaril, administered either orally or intranasally, is active against viruses in the Picornaviridae family, including Enterovirus and Rhinovirus. It has shown useful activity against the dangerous enterovirus D68.
This family represents the internal ribosome entry site (IRES) of the hepatitis A virus. HAV IRES is a 450 nucleotide long sequence located in the 735 nt long 5’ UTR of Hepatitis A viral RNA genome. IRES elements allow cap and end-independent translation of mRNA in the host cell. The IRES achieves this by mediating the internal initiation of translation by recruiting a ribosomal 40S pre-initiation complex directly to the initiation codon and eliminates the requirement for eukaryotic initiation factor, eIF4F.
Vincent R. Racaniello is a Higgins Professor in the Department of Microbiology and Immunology at Columbia University's College of Physicians and Surgeons. He is a co-author of a textbook on virology, Principles of Virology.
Enterovirus E is a picornavirus of the genus Enterovirus. The virus may also be referred to as enteric cytopathic bovine orphan virus (ECBO). It is endemic in cattle populations worldwide, and although normally fairly nonpathogenic, it can cause reproductive, respiratory, or enteric disease – particularly when the animal is concurrently infected with another pathogen.
Iflaviridae is a family of positive sense RNA viruses insect-infecting viruses. Some of the insects commonly infected by iflaviruses include aphids, leafhoppers, flies, bees, ants, silkworms and wasps. The name "Ifla" is derived from the name "Infectious flacherie virus", a member species. There is one genus (Iflavirus) and 16 species in this family.
Cripavirus is a genus of viruses in the order Picornavirales, in the family Dicistroviridae. Invertebrates serve as natural hosts. There are four species in this genus. Diseases associated with this genus include: DCV: increased reproductive potential; extremely pathogenic when injected with high associated mortality; CrPV: paralysis and death. These viruses can produce proteins directly from their RNA genome upon entering a cell; and therefore, does not require an RNA polymerase packaged in with it, as this may be produced from the genome after entering the cell. The name of the cripavirus family originates from its most famous member the Cricket Paralysis Virus. Which was made famous by its rather unusual IRES : the Cripavirus IRES. The Cripavirus IRES is an RNA element that allows the virus to bind the ribosome and translate without a need for any initiation factors – as initiation is the most regulated step of translation this allows the virus to avoid many mechanisms to inhibit viral activity.
Picornain 3C is a protease found in picornaviruses, which cleaves peptide bonds of non-terminal sequences. Picornain 3C’s endopeptidase activity is primarily responsible for the catalytic process of selectively cleaving Gln-Gly bonds in the polyprotein of poliovirus and with substitution of Glu for Gln, and Ser or Thr for Gly in other picornaviruses. Picornain 3C are cysteine proteases related by amino acid sequence to trypsin-like serine proteases. Picornain 3C is encoded by enteroviruses, rhinoviruses, aphtoviruses and cardioviruses. These genera of picoviruses cause a wide range of infections in humans and mammals.
Rhopalosiphum padi virus (RhPV) is a member of Dicistroviridae family, which includes cricket paralysis virus (CrPV), Plautia stali intestine virus and Drosophila C virus. Its 5'UTR region contains an internal ribosome entry site (IRES) element with a cross-kingdom activity. It can function efficiently in mammalian, plant and insect translation systems. Testing of R. padi aphids collected from different sites in Sweden revealed the presence of RhPV in wild aphid populations for the first time in Europe. Virus could be detected in several life stages of R. padi, including sexual individuals and eggs, establishing an over-wintering route for the virus.
Triatoma virus (TrV) is a virus belonging to the insect virus family Dicistroviridae. Within this family, there are currently 3 genera and 15 species of virus. Triatoma virus belongs to the genus Cripavirus. It is non-enveloped and its genetic material is positive-sense, single-stranded RNA. The natural hosts of triatoma virus are invertebrates. TrV is a known pathogen to Triatoma infestans, the major vector of Chagas disease in Argentina which makes triatoma virus a major candidate for biological vector control as opposed to chemical insecticides. Triatoma virus was first discovered in 1984 when a survey of pathogens of triatomes was conducted in the hopes of finding potential biological control methods for T. infestans.
The black queen cell virus (BQCV) is a virus that infects honey bees, specifically Apis mellifera, Apis florea, and Apis dorsata. Infection of the latter two species is more recent and can be attributed to genetic similarity and geographical closeness.
Black beetle virus (BBV) is a virus that was initially discovered in the North Island of New Zealand in Helensville in dead New Zealand black beetles in 1975.