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| Parvovirus |
| Virus classification |
| Group: |
ii single-stranded DNA |
| Family: |
Parvoviridae |
Parvovirus is the common name applied to all the viruses in the Parvoviridae taxonomic family.
Parvoviruses are linear, non-segmented single-stranded DNA viruses, with an average genome size of 5000 nucleotides. Parvoviruses are among the smallest viruses (hence the name, from Latin parvus meaning small) and are 18–28 nm in diameter.[1]
Parvoviruses can cause disease in some animals. Because the viruses require actively dividing cells in order to replicate, the type of tissue infected varies with the age of the animal. The gastrointestinal tract and lymphatic system can be affected at any age, leading to vomiting, diarrhea and immunosuppression but cerebellar hypoplasia is only seen in cats that were infected in the womb or at less than two weeks of age, and disease of the myocardium is seen in puppies infected between the ages of three and eight weeks.[2]
Contents
- 1 Structure
- 2 Disease information on Parvoviridae
- 2.1 Diseases caused by members of the Parvoviridae family
- 2.2 Replication as disease vector
- 3 Use of HeLa cells in parvo virus testing
- 4 See also
- 5 References
- 6 Further reading
- 7 External links
Structure
The viral capsid of a parvovirus is made up of two to four proteins, known as VP1-4 that form an icosahedral structure that is resistant to acids, bases, solvents and temperature up to 50 °C (122 degrees Fahrenheit).
Inside the capsid is a single-stranded DNA genome. At the 5’ and 3’ ends of this genome are palindromic sequences of approximately 120 to 250 nucleotides, that form hairpins and are essential for viral genome replication.
Disease information on Parvoviridae
The remainder of this article discusses the disease-causing Parvoviridae viri, rather than the members of the Parvovirus genus.
Diseases caused by members of the Parvoviridae family
Micrograph showing a parvovirus infected nucleated (fetal) red blood cells. H&E stain.
See also: Parvovirus B19 and Canine parvovirus
Parvovirus B19, which causes fifth disease in humans, is a member of the Erythrovirus genus of the Parvoviridae.
Prior to 2014, it was also the name applied to a genus within the subfamily Parvovirinae, but this has been amended to genus Protoparvovirus to avoid confusion between taxonomic levels.[3][4] Parvoviruses that infect vertebrate hosts make up the subfamily Parvovirinae, while those that infect arthropods (currently only known to infect insects or shrimp) make up the subfamily Densovirinae.
Many mammalian species sustain infection by multiple parvoviruses. Parvoviruses tend to be specific about the species of animal they will infect, but this is a somewhat flexible characteristic. Thus, all isolates of canine parvovirus affect dogs, wolves, and foxes, but only some of them will infect cats.
Humans can be infected by viruses from five of the eight genera in the subfamily Parvovirinae: i) Bocaparvovirus (e.g. human bocavirus 1), ii) Dependoparvovirus (e.g. adeno-associated virus 2), iii) Erythroparvovirus (e.g. parvovirus B19), iv) Protoparvovirus (e.g. bufavirus 1a) and v) Tetraparvovirus (e.g. human parv4 G1). As of 2014, there were no known human viruses in the remaining three recognized genera: vi) Amdoparvovirus (e.g. Aleutian mink disease virus), vii) Aveparvovirus (e.g. chicken parvovirus) and viii) Copiparvovirus (e.g. bovine parvovirus 2).
Canine parvovirus is a particularly deadly disease among young puppies, about 80% fatal, causing gastrointestinal tract damage and dehydration as well as a cardiac syndrome in very young pups. It is spread by contact with an infected dog's feces. Symptoms include lethargy, severe diarrhea, fever, vomiting, loss of appetite, and dehydration.
Mouse parvovirus 1, however, causes no symptoms but can contaminate immunology experiments in biological research laboratories.
Porcine parvovirus causes a reproductive disease in swine known as SMEDI, which stands for stillbirth, mummification, embryonic death, and infertility.
Feline panleukopenia is common in kittens and causes fever, low white blood cell count, diarrhea, and death. Infection of the cat fetus and kittens less than two weeks old causes cerebellar hypoplasia.
Mink enteritis virus is similar in effect to feline panleukopenia, except that it does not cause cerebellar hypoplasia. A different parvovirus causes Aleutian Disease in minks and other mustelids, characterized by lymphadenopathy, splenomegaly, glomerulonephritis, anemia, and death.
The most accurate diagnosis of parvovirus is by ELISA.
Dogs, cats and swine can be vaccinated against parvovirus.
Replication as disease vector
To enter host cells, parvoviruses bind to a sialic acid-bearing cell surface receptor. Penetration into the cytoplasm is mediated by a phospholipase A2 activity carried on the amino-terminal peptide of the capsid VP1 polypeptide. Once in the cytoplasm, the intact virus is translocated to the nucleus prior to uncoating. Transcription only initiates when the host cell enters S-phase under its own cell cycle control, at which time the cell's replication machinery converts the incoming single strand into a duplex transcription template, allowing synthesis of mRNAs encoding the non-structural proteins, NS1 and NS2. The mRNAs are transported out of the nucleus into the cytoplasm where the host ribosomes translate them into viral proteins. Viral DNA replication proceeds through a series of monomeric and concatemeric duplex intermediates by a unidirectional strand-displacement mechanism that is mediated by components of the host replication fork, aided and orchestrated by the viral NS1 polypeptide. NS1 also transactivates an internal transcriptional promoter that directs synthesis of the structural VP polypeptides. Once assembled capsids are available, replication shifts from synthesizing duplex DNA to displacement of progeny single strands, which are typically negative-sense and are packaged in a 3'-to-5' direction into preformed particles within the nucleus. Mature virions may be released from infected cells prior to cell lysis, which promotes rapid transmission of the virus, but if this fails then the virus is released at cell lysis.
Unlike most other DNA viruses, parvoviruses are unable to activate DNA synthesis in host cells. Thus, in order for viral replication to take place the infected cells must be non-quiescent (i.e. must be actively mitotic). Their inability to force host cells into S-phase means that parvoviruses are non-tumorigenic. Indeed they are commonly oncolytic, showing a strong tendency to replicate preferentially in cells with transformed phenotypes.
Use of HeLa cells in parvo virus testing
Testing for how feline parvo virus and canine parvo virus infect cells and what pathways are taken; scientists used cat cells, mouse cells, cat and mouse hybrid cells, mink cells, dog cells, human cells, and HeLa cells.[5] Both feline parvo virus and canine parvo virus enter their hosts, follow specific pathways, and infect at certain parts of cells before infecting major organs. Parvo viruses are specific viruses that are determined by what receptors they attack.[6] Testing found that parvo virus infects carnivorous animals through the oropharyngeal pathway. Parvo virus infects the oropharyngeal cells that come in immediate contact with the virus. Parvo virus contains a plasmid that infects and binds to transferrin receptors, a glycoprotein, on the plasma membrane.[7][8] The parvo virus plasmid is stored in a small non- enveloped capsid.[7][9] Once oropharyngeal cells become infected the virus spreads to dividing lymph cells and continues to work to the bone marrow and spread to target organs through blood.
Testing of HeLa cells and human cells to exposure of both feline parvo virus and canine parvo virus resulted in infections of the cells at human transferrin receptors.[5] When anti-bodies and parvo virus samples were added at the same time to human cells and HeLa cells it was found that no infection would take place; experiments showed that both human cells and HeLa cells have transferrin receptors but there is no evidence of humans contracting parvo virus.
Certain chromosomes in cells show more susceptibility to parvo virus than others. Testing of feline parvo virus on cat cells and cat mouse hybrid cells found cultures with cells having the highest concentrations of the C2 chromosome were the most highly infected cells.[5] Slight mutations of binding sites were found to slow down or completely stop the infection of the given parvo virus; whereas cells that are naturally missing the receptors or are mutated to not have them cannot be mutated.[8] Both feline parvo virus and canine parvo virus express plasticity during cellular infection.[9][10] Although transferrin receptors may be limited on cell surfaces the parvo viruses will find available transferrin receptors and will use different pathways to gain entry to the cells plasma membrane. Unlike plasma membrane infection plasticity, all strains of parvo virus show related routes to the cell nucleus.
Canine parvo virus is a mutated strain of feline parvo virus.[5][6][7] The conditions needed for the mutation had to be perfect for the virus to change species of infection. The mutation occurred in the capsid proteins of feline parvo virus that gave it the ability to infect dogs.[8] Both viruses remain similar so once the mutation occurred strains of canine parvo virus had a tradeoff of becoming more receptive to canine cells and less receptive to feline cells; only mutated feline parvo virus, the canine parvo virus, can infect both species of cats and dogs cells but standard un- mutated feline parvo virus can only infect feline cells. Both feline parvo virus and canine parvo virus bind to and infect the transferrin receptors but both have different sequences in the cells and animals. Infection by both feline parvo virus and canine parvo virus are relatively quick; but because of constant mutation of canine parvo virus, canine parvo virus has a slower infection time than feline parvo virus.[9] Studies of other strains of mutated canine parvo virus have revealed that changes in the viral capsid by just one protein can be fatal to the virus. Wrong mutations have been noted to lead to inability to bind to transferrin receptors, bind to non- receptive parts of the cell membrane, and identification of the virus by the host’s antibody cells.[10]
See also
References
- ^ Leppard, Keith; Nigel Dimmock; Easton, Andrew (2007). Introduction to Modern Virology. Blackwell Publishing Limited. p. 450. ISBN 1-4051-3645-6.
- ^ Fenner, Frank J.; Gibbs, E. Paul J.; Murphy, Frederick A.; Rott, Rudolph; Studdert, Michael J.; White, David O. (1993). Veterinary Virology (2nd ed.). Academic Press, Inc. ISBN 0-12-253056-X.
- ^ Cotmore SF, Agbandje-McKenna M, Chiorini JA, Mukha DV, Pintel DJ, et al. 2014. The family Parvoviridae. Arch. Virol. 159:1239--47.
- ^ http://talk.ictvonline.org/files/ictv_official_taxonomy_updates_since_the_8th_report/m/vertebrate-official/4844.aspx
- ^ a b c d Parker, J; Murphy W; Wang D; O'Brien S; Parrish C (2001). "Canine and feline parvoviruses can use human or feline transferrin receptors to bind, enter, and infect cells". Journal of Virology 75 (8): 3896–3902. doi:10.1128/JVI.75.8.3896-3902.2001. PMC 114880. PMID 11264378. Retrieved 3 April 2012.
- ^ a b Ross, S; Schofield J; Farr C; Bucan M (2002). "Mouse transferrin receptor 1 is the cell entry receptor for mouse mammary tumor virus". Proceedings of the National Academy of Sciences of the United States of America 99 (19): 12386–12390. doi:10.1073/pnas.192360099.
- ^ a b c Heuffer, K; Parker J; Weichert W; Geisel R; Sgro J; Parrish C (2003). "The natural host range shift and subsequent evolution of canine parvovirus resulted from virus-specific binding to the canine transferrin receptor". Journal of Virology 77 (3): 1718–1726.
- ^ a b c Goodman, L; Lyi A; Johnson N; Cifuente J; Hafenstein S; Parrish C (2010). "Binding site on the transferrin receptor for the parvovirus capsid and effects of altered affinity on cell uptake and infection". Journal of Virology 84 (10): 4969–4978. doi:10.1128/jvi.02623-09.
- ^ a b c Harbison, C; Lyi S; Weichert W; Parrish C (2009). "Early steps in cell infection by parvoviruses: host-specific differences in cell receptor binding but similar endosomal trafficking". Journal of Virology 83 (20): 10504–10514. doi:10.1128/jvi.00295-09.
- ^ a b Nelson, C; Minkkinen E, Bergkvist M, Hoelzer K, Fisher M, Bothner B, Parrish (2008). "Detecting small changes and additional peptides in the canine parvovirus capsid structure". Journal of Virology 82 (21): 10397–10407. doi:10.1128/jvi.00972-08.
Further reading
Feline Parvovirus by Cats Protection
External links
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Microbiology: Virus
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| Components |
- Viral envelope
- Capsid
- Viral protein
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| Viral life cycle |
- Viral entry
- Viral replication
- Viral shedding
- Virus latency
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| Genetics |
- Reassortment
- Antigenic shift
- Antigenic drift
- Phenotype mixing
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| Other |
- Viral disease
- Laboratory diagnosis of viral infections
- Viral load
- Viral quantification
- Antiviral drug
- Bacteriophage
- Neurotropic virus
- Oncovirus
- History of viruses
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cutn/syst (hppv/hiva, infl/zost/zoon)/epon
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drug (dnaa, rnaa, rtva, vacc)
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