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Parvovirus, commonly truncated to parvo, is a genus of the Parvoviridae family linear, non-segmented single stranded DNA viruses with an average genome size of 5 kbp. Parvoviruses are some of the smallest viruses found in nature (hence the name, from Latin parvus meaning small). Some have been found as small as 23nm.
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 from three other genera from the Family Parvoviridae. These are the Dependoviruses (e.g. Adeno-Associated Virus), the Erythroviruses (e.g. Parvovirus B19) and the Bocaviruses.
The viral capsid of parvovirus is made up of 2-3 proteins known as VP1-3 that form an icosahedral structure that is resistant to pH, 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 120-250 nucleotides that form hairpins and are essential for viral genome replication.
In order 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 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.
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