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Virus classification
Group: ii single-stranded DNA
Family: Parvoviridae


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]


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[edit]

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[edit]

Micrograph showing a parvovirus infected nucleated (fetal) red blood cells. H&E stain.


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.



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.




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[edit]



Use of HeLa cells in parvo virus testing[edit]

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[edit]


  1. ^ Leppard, Keith; Nigel Dimmock; Easton, Andrew (2007). Introduction to Modern Virology. Blackwell Publishing Limited. p. 450. ISBN 1-4051-3645-6. 
  3. ^ Cotmore SF, Agbandje-McKenna M, Chiorini JA, Mukha DV, Pintel DJ, et al. 2014. The family Parvoviridae. Arch. Virol. 159:1239--47.
  4. ^
  5. ^ 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. 
  6. ^ 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. 
  7. ^ 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. 
  8. ^ 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. 
  9. ^ 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. 
  10. ^ 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[edit]

Feline Parvovirus by Cats Protection

External links[edit]