Parvovirus

Parvovirus, often truncated to "parvo", is both the common name in English casually applied to all the viruses in the Parvoviridae taxonomic family, and also the taxonomic name of the Parvovirus genus within the Parvoviridae family. This creates a confusion of terms, because parvoviruses which causes human and animal diseases are not in genus Parvovirus though they are casually called parvoviruses just as lions and tigers are sometimes called "cats," being also felids. Parvoviruses are typically linear, non-segmented single-stranded DNA viruses, with an average genome size of 5000 nucleotides. Parvoviruses are some of the smallest viruses (hence the name, from Latin parvus meaning small) and are 18–26 nm in diameter.

Many types of mammalian species have a strain of parvovirus associated with them. Parvoviruses tend to be specific about the taxon of animal they will infect, but this is a somewhat flexible characteristic. Thus, all strains of canine parvovirus will affect dogs, wolves, and foxes, but only some of them will infect cats.

No members of the genus Parvovirus are currently known to infect humans, but humans can be infected by viruses within three other genera from the family Parvoviridae, including the one popularly known by the common name Parvovirus B19. These are the Dependoviruses (e.g. Adeno-Associated Virus), the Erythroviruses (e.g. Parvovirus B19) and the Bocaviruses.

Structure
The viral capsid of parvovirus is made up of two or three proteins, known as VP1-3 that form an icosahedral structure that is resistant to acids, bases, solvents and temperature up to 50°C.

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 from Parvoviridae family (but not Parvovirus genus)


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.

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.

Parvovirus B19, which causes fifth disease in humans, is a member of the Erythrovirus genus of the Parvoviridae.

In humans the P antigen (also known as globoside) is the cellular receptor for parvovirus B19 virus that causes Erythema infectiosum (fifth disease) in children. This infection is sometimes complicated by severe aplastic anemia caused by lysis of early erythroid precursors.

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 cellular 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 turn on 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.