Parvoviruses are a family of animal viruses that constitute the family Parvoviridae. They have linear, single-stranded DNA (ssDNA) genomes that typically contain two genes encoding for a replication initiator protein, called NS1, and the protein the viral capsid is made of. The coding portion of the genome is flanked by telomeres at each end that form into hairpin loops that are important during replication. Parvovirus virions are small compared to most viruses, at 23–28 nanometers in diameter, and contain the genome enclosed in an icosahedral capsid that has a rugged surface.
Parvoviruses enter a host cell by endocytosis, travelling to the nucleus where they wait until the cell enters its replication stage. At that point, the genome is uncoated and the coding portion is replicated. Viral messenger RNA (mRNA) is then transcribed and translated, resulting in NS1 initiating replication. During replication, the hairpins repeatedly unfold, are replicated, and refold to change the direction of replication to progress back and forth along the genome in a process called rolling hairpin replication that produces a molecule containing numerous copies of the genome. Progeny ssDNA genomes are excised from this concatemer and packaged into capsids. Mature virions leave the cell by exocytosis or lysis.
Parvoviruses are believed to be descended from ssDNA viruses that have circular genomes that form a loop because these viruses encode a replication initiator protein that is related to NS1 and have a similar replication mechanism. Another group of viruses called bidnaviruses appear to be descended from parvoviruses. Within the family, three subfamilies, 26 genera, and 126 species are recognized. Parvoviridae is the sole family in the order Piccovirales, which is the sole order in the class Quintoviricetes. This class is assigned to the phylum Cossaviricota, which also includes papillomaviruses, polyomaviruses, and bidnaviruses.
A variety of diseases in animals are caused by parvoviruses. Notably, the canine parvovirus and feline parvovirus cause severe disease in dogs and cats, respectively. In pigs, the porcine parvovirus is a major cause of infertility. Human parvoviruses are less severe, the two most notable being parvovirus B19, which causes a variety of illnesses including fifth disease in children, and human bocavirus 1, which is a common cause of acute respiratory tract illness, especially in young children. In medicine, recombinant adeno-associated viruses (AAV) have become an important vector for delivering genes to the cell nucleus during gene therapy.
Animal parvoviruses were first discovered in the 1960s, including minute virus of mice, which is frequently used to study parvovirus replication. Many AAVs were also discovered during this time period and research on them over time has revealed their benefit as a form of medicine. The first pathogenic human parvovirus to be discovered was parvovirus B19 in 1974, which became associated with various diseases throughout the 1980s. Parvoviruses were first classified as the genus Parvovirus in 1971 but were elevated to family status in 1975. They take their name from the Latin word parvum, meaning 'small' or 'tiny', referring to the small size of the virus's virions.
Genome
Parvoviruses have linear, single-stranded DNA (ssDNA) genomes that are about 4–6 kilobases (kb) in length. The parvovirus genome typically contains two genes, termed the NS/rep gene and the VP/cap gene.[1] The NS gene encodes the non-structural (NS) protein NS1, which is the replication initiator protein, and the VP gene encodes the viral protein (VP) that the viral capsid is made of. NS1 contains an HUH superfamilyendonuclease domain near its N-terminus, containing both site-specific binding activity and site-specific nicking activity, and a superfamily 3 (SF3) helicase domain toward the C-terminus. Most parvoviruses contain a transcriptional activation domain near the C-terminus that upregulates transcription from viral promoters as well as alternate or overlapping open reading frames that encode a small number of supporting proteins involved in different aspects of the viral life cycle.[2]
The coding portion of the genome is flanked at each end by terminal sequences about 116–550 nucleotides (nt) in length that consist of imperfect palindromes folded into hairpin loop structures. These hairpin loops contain most of the cis-acting information required for DNA replication and packaging and act as hinges during replication to change the direction of replication. When the genome is converted to double-stranded forms, replication origin sites are created involving sequences in and adjacent to the hairpins.[2][3]
Genomic DNA strands in mature virions may be positive-sense or negative-sense. This varies from species to species as some have a preference for packaging strands of one polarity, others package varying proportions, and others package both sense strands at equal proportions. These preferences reflect the efficiency with which progeny strands are synthesized, which in turn reflects the efficiency of specific replication origin sites.[2] The 3′-end (usually pronounced "three prime end") of a negative sense strand, and the 5′-end (usually pronounced "five prime end") of a positive sense strand, is called the left end, and the 5′-end of the negative sense strand, and the 3′-end of a positive sense strand, is called the right end.[2][4][5]
Structure
Schematic diagram of a ParvoviridaevirionA diagram of the canine parvovirus's capsid, containing 60 monomers of the capsid protein.
Parvovirus virions are 23–28 nanometers (nm) in diameter and consist of the genome enclosed inside a capsid that is icosahedral in shape with a rugged surface. The capsid is composed of 60 structurally equivalent polypeptide chains derived from the C-terminal end of a VP protein's sequence, interlocking extensively to form an icosahedron with 60 asymmetric, superficial triangular units. These units have 3-fold radial symmetry at two vertices and 5-fold radial symmetry at one, with 2-fold radial symmetry at the line opposite of the 5-fold vertex and a 2/5 circular fold wall surrounding the point of the 5-fold vertex. Twenty 3-fold vertices, thirty 2-fold lines, and twelve 5-fold vertices exist per capsid, the latter corresponding to the 12 vertices of the icosahedron.[2]
Typical features of the capsid surface include depressions at each 2-fold axis, elevated protrusions surrounding the 3-fold axes, and raised cylindrical projections made of five beta-barrels[6] surrounded by canyon-like depressions at the 5-fold axes. Each of these cylinders potentially contains an opening to connect the exterior of the capsid to the interior, which mediates entry and exit of the genome. About 20 nucleotides from the 5′-end of the genome may remain exposed outside of the capsid carrying a copy of NS1 bound to the 5′-end, which is a result of how the genome is synthesized and packaged.[2]
Varying sizes of the VP protein are expressed for different parvoviruses, the smaller ones, VP2–5, being expressed at a higher frequency than the large size, VP1. The smaller VPs share a common C-terminus with different N-terminus lengths due to truncation. For VP1, the N-terminus is extended to contain regions important in the replication cycle, and it is incorporated into the capsid, typically 5–10 per capsid, with the common C-terminus responsible for assembling capsids.[1][2]
Each VP monomer contains a core beta-barrel structure called the jelly roll motif of eight strands arranged in two adjacent antiparallel beta sheets, labeled CHEF and BIDG after the individual strands, the latter forming the interior surface of the capsid. Individual beta strands are connected by loops that have varying length, sequence, and conformation, and most of these loops extend toward the exterior surface, giving parvoviruses their unique, rough surface. Related parvoviruses share their surface topologies and VP protein folds to a greater degree than their sequence identities, so the structure of the capsid and capsid protein are useful indicators of phylogeny.[1][2]
Life cycle
Parvoviruses enter cells by endocytosis, using a variety of cellular receptors to bind to the host cell. In endosomes, many parvoviruses undergo a change in conformation so that the phospholipase A2 (PLA2) domain on the VP1 N-termini are exposed so the virion can penetrate lipid bilayer membranes. Intracellular trafficking of virions varies, but virions ultimately arrive to the nucleus, inside of which the genome is uncoated from the capsid. Based on studies of minute virus of mice (MVM), the genome is ejected from the capsid in a 3′-to-5′ direction from one of the openings in the capsid, leaving the 5′-end of the DNA attached to the capsid.[2]
Parvoviruses lack the ability to induce cells into their DNA replication stage, called S-phase, so they must wait in the nucleus until the host cell enters S-phase on its own. This makes cell populations that divide rapidly, such as fetal cells, an excellent environment for parvoviruses. Adeno-associated viruses (AAV) are dependent on helper viruses, which may be an adenovirus or a herpesvirus, since coinfection alters the cellular environment to allow for replication.[2] In the absence of coinfection, AAV's genome is integrated into the host cell's genome until coinfection occurs.[7] Infected cells that enter S-phase are forced to synthesize viral DNA and cannot leave S-phase. Parvoviruses establish replication foci in the nucleus that grow progressively larger as infection progresses.[8]
Once a cell enters S-phase and the genome is uncoated, a host DNA polymerase uses the 3′-end of the 3′ hairpin as a primer to synthesize a complementary DNA strand for the coding portion of the genome, which is connected to the 5′-end of the 5′ hairpin.[3][7][9]Messenger RNA (mRNA) that encodes NS1 is then transcribed from the genome by the DNA polymerase, capped and polyadenylated, and translated by host ribosomes to synthesize NS1.[2][5][10] If proteins are encoded in multiple co-linear frames, then alternative splicing, suboptimal translation initiation, or leaky scanning may be used to translate different gene products.[2]
Parvoviruses replicate their genome via rolling hairpin replication, a unidirectional, strand displacement form of DNA replication that is initiated by NS1. Replication begins once NS1 binds to and makes a nick in a replication origin site in the duplex DNA molecule at the end of one hairpin. Nicking releases the 3′-end of the nicked strand as a free hydroxyl (-OH) to prime DNA synthesis[2] with NS1 remaining attached to the 5′-end.[7] The nick causes the adjacent hairpin to unfold into a linear, extended form. At the 3′-OH, a replication fork is established using NS1's helicase activity, and the extended telomere is replicated by the DNA polymerase.[10][11] The two telomere strands then refold back in on themselves to their original configurations, which repositions the replication fork to switch templates to the other strand and move in the opposite direction toward the other end of the genome.[12][13]
Parvoviruses vary in whether the termini are similar or the same, called homotelomeric parvoviruses, or different, called heterotelomeric parvoviruses. In general, homotelomeric parvoviruses, such as AAV and B19, replicate both ends of their genome through the aforementioned process, called terminal resolution, and their hairpin sequences are contained within larger (inverted) terminal repeats. Heterotelomeric viruses, such as minute virus of mice (MVM), replicate one end by terminal resolution and the other end via an asymmetric process called junction resolution[2][14] so that the correct orientation of the telomere can be copied.[15]
During asymmetric junction resolution, the duplex extended-form telomeres refold in on themselves into a cruciform shape. A replication origin site on the lower strand of the right arm of the cruciform is nicked by NS1, leading to the lower arm of the cruciform unfolding into its linear extended form. A replication fork established at the nick site moves down the extended lower arm to copy the lower arm's sequence. The two strands of the lower arm then refold to reposition the replication fork to go back toward the other end, displacing the upper strand in the process.[16]
The back and forth, end-to-end pattern of rolling hairpin replication produces a concatemer containing multiple copies of the genome.[2][3] NS1 periodically makes nicks in this molecule and, through a combination of terminal resolution and junction resolution, individual strands of the genome are excised from the concatemer.[9][13] Excised genomes may either be recycled for further rounds of replication or packaged into progeny capsids.[7] Translation of mRNA containing VP proteins leads to the accumulation of capsid proteins in the nucleus that assemble into these empty capsids.[8]
Genomes are encapsidated at one of the capsid's vertices through a portal,[2] potentially the one opposite the portal used to expel the genome.[5] Once complete virions have been constructed, they may be exported from the nucleus to the exterior of the cell before disintegration of the nucleus. Disruption of the host cell environment may also occur later on in the infection. This results in cell lysis via necrosis or apoptosis, which releases virions to the outside of the cell.[2][8]
Evolution
Parvoviruses are believed to be descended from ssDNA viruses that have a circular genome that forms a loop and which replicate via rolling circle replication, which is similar to rolling hairpin replication. These circular ssDNA viruses encode a replication initiator protein that is related to and possesses many of the same characteristics as the replication initiator protein of parvoviruses, such as the HUH endonuclease domain and the SF3 helicase domain.[17] In contrast to these other replication initiator proteins, NS1 shows only vestigial traces of being able to perform ligation, which is a key part of rolling circle replication.[8] The Bidnaviridae family, which are also linear ssDNA viruses, appear to be descended from a parvovirus that had its genome integrated into the genome of a polinton, a type of DNA transposon related to viruses in the realm Varidnaviria.[17]
Based on phylogenetic analysis of the SF3 helicase, parvoviruses split into two branches early in their evolutionary history, one of which contains viruses assigned to the subfamily Hamaparvovirinae. The other branch split into two sublineages that constitute the other two subfamilies, Densovirinae and Parvovirinae.[18] Parvoviruses in the Hamaparvovirinae lineage are likely all heterotelomeric, Densovirinae are exclusively homotelomeric, and Parvovirinae varies.[2] Telomere sequences have significant complexity and diversity, suggesting that many species have co-opted them to perform additional functions.[7][10] Parvoviruses are also considered to have high rates of genetic mutations and recombinations.[2][9]
Classification
Parvoviruses constitute the family Parvoviridae. The family is the sole family in the order Piccovirales, which is the sole order in the class Quintoviricetes. The class Quintoviricetes belongs to the phylum Cossaviricota, which also includes papillomaviruses, polyomaviruses, and bidnaviruses. Cossaviricota is included in the kingdom Shotokuvirae, which is assigned to the realm Monodnaviria. Parvoviridae belongs to Group II: ssDNA viruses in the Baltimore classification system, which groups viruses together based on their manner of mRNA synthesis. Within Parvoviridae, three subfamilies, 26 genera, and 126 species are recognized as of 2020 (-virinae denotes subfamily and -virus denotes genus):[18][19]
Parvoviruses are assigned to the same species if they share at least 85% of their protein sequence identities. Species are grouped together in a genus based on phylogeny of the NS1 and SF3 helicase domains, as well as similarity of NS1 sequence identity and coverage. If these criteria aren't satisfied, then genera can still be established provided that common ancestry is supported. The three subfamilies are distinguished based on phylogeny of the SF3 helicase domain, which corresponds to host range: viruses in Densovirinae infect invertebrates, viruses in Hamaparvovirinae infect invertebrates and vertebrates, and viruses in Parvovirinae infect vertebrates.[18]
Disease
Child with Fifth disease
In humans, the most prominent parvoviruses that cause disease are parvovirus B19 and human bocavirus 1. B19 infection is often asymptomatic but can manifest in a variety of ways, including Fifth disease with its characteristic rash in children, persistent anemia in immunocompromised persons and in people who have underlying hemoglobinopathies,[20] transient aplastic crises, hydrops fetalis in pregnant women, and arthropathy. Human bocavirus 1 is a common cause of acute respiratory tract infection, especially in young children, wheezing being a common symptom. Other parvoviruses associated with different diseases in humans include human parvovirus 4 and human bufavirus, though the manner by which these viruses cause disease is unclear.[6]
Carnivore-infecting viruses in the genus Protoparvovirus, in contrast to human parvoviruses, are more life-threatening.[2]Canine parvovirus causes severe illness in dogs, the most common symptom being hemorrhagic enteritis, with up to a 70% mortality rate in pups but usually less than 1% in adults.[21]Feline parvovirus, a closely related virus,[22] likewise causes severe illness in cats along with panleukopenia.[23][24] In pigs, porcine parvovirus is a major cause of infertility as infection frequently leads to death of the fetus.[25]
Use in medicine
Adeno-associated viruses have become an important vector for gene therapy aimed at treating genetic diseases, such as those caused by a single mutation. The recombinant AAV (rAAV) contains a viral capsid but lacks a complete viral genome. Instead, the typical nucleic acid packaged into the capsid contains a promoter region, the gene of interest, and a terminator region, all contained within two inverted terminal repeats derived from the viral genome. rAAV essentially acts as a container that can traverse the cell membrane and deliver its nucleic acid cargo to the nucleus.[26][27]
History
Parvoviruses were discovered relatively late in comparison to other prominent virus families, potentially due to their small size. In the late 1950s[28] and 1960s,[29] a variety of animal parvoviruses were discovered, including minute virus of mice,[30] which has since been used extensively to study rolling hairpin replication.[31] Many AAVs were also discovered during this time period[32] and research on them led to their first usage in gene therapy in the 1980s. Over time, improvements in aspects such as vector design led to certain AAV gene therapy products reaching clinical efficacy in 2008 and being approved in the following years.[27]
In 1974, the first pathogenic human parvovirus was discovered by Yvonne Cossart, et al. When testing for the hepatitis B virus's surface antigen, one serum sample gave anomalous results and with electron microscopy was shown to contain a virus resembling animal parvoviruses. This virus was named B19 after the coding of the serum sample, number 19 in panel B.[20][33] B19 was later recognized as a species by the International Committee on Taxonomy of Viruses (ICTV) in 1985, and throughout the 1980s it increasingly became associated with various diseases.[33]
In the ICTV's first report in 1971, parvoviruses were grouped together in the genus Parvovirus.[30][32] They were elevated to the rank of family in 1975 and remained unassigned to higher taxa until 2019, when they were assigned to higher taxa up to the highest rank, realm.[34] The family was reorganized in 2019, departing from the "traditional" invertebrate-vertebrate distinction between Densovirinae and Parvovirinae and instead distinguishing the subfamilies based on helicase phylogeny, leading to the establishment of a new subfamily, Hamaparvovirinae.[18]
Etymology
Parvoviruses take their name from Latinparvus or parvum, meaning small or tiny, referring to the small size of parvovirus virions compared to most other viruses.[2][20] In the family name Parvoviridae, -viridae is the suffix used for virus families.[35] The order Piccovirales takes the first part of its name from the Italian word piccolo, meaning small, and the second part is the suffix used for virus orders. The class Quintoviricetes takes the first part of its name from the Galician word quinto, meaning fifth, referring to fifth disease (erythema infectiosum) caused by parvovirus B19, and viricetes, the suffix used for virus classes.[17]
A DNA virus is a virus that has a genome made of deoxyribonucleic acid (DNA) that is replicated by a DNA polymerase. They can be divided between those that have two strands of DNA in their genome, called double-stranded DNA (dsDNA) viruses, and those that have one strand of DNA in their genome, called single-stranded DNA (ssDNA) viruses. dsDNA viruses primarily belong to two realms: Duplodnaviria and Varidnaviria, and ssDNA viruses are almost exclusively assigned to the realm Monodnaviria, which also includes some dsDNA viruses. Additionally, many DNA viruses are unassigned to higher taxa. Reverse transcribing viruses, which have a DNA genome that is replicated through an RNA intermediate by a reverse transcriptase, are classified into the kingdom Pararnavirae in the realm Riboviria.
Hepadnaviridae is a family of viruses. Humans, apes, and birds serve as natural hosts. There are currently 18 species in this family, divided among 5 genera. Its best-known member is hepatitis B virus. Diseases associated with this family include: liver infections, such as hepatitis, hepatocellular carcinomas, and cirrhosis. It is the sole accepted family in the order Blubervirales.
Human parvovirus B19, generally referred to as B19 virus(B19V),parvovirus B19 or sometimes erythrovirus B19, is the first known human virus in the family Parvoviridae, genus Erythroparvovirus; it measures only 23–26 nm in diameter. Human parvovirus b19 is a below-species classification of Erythroparvovirus primate1. The name is derived from Latin parvum, meaning small, reflecting the fact that B19 ranks among the smallest DNA viruses. B19 virus is most known for causing disease in the pediatric population; however, it can also affect adults. It is the classic cause of the childhood rash called fifth disease or erythema infectiosum, or "slapped cheek syndrome".
Adeno-associated viruses (AAV) are small viruses that infect humans and some other primate species. They belong to the genus Dependoparvovirus, which in turn belongs to the family Parvoviridae. They are small replication-defective, nonenveloped viruses and have linear single-stranded DNA (ssDNA) genome of approximately 4.8 kilobases (kb).
Baltimore classification is a system used to classify viruses based on their manner of messenger RNA (mRNA) synthesis. By organizing viruses based on their manner of mRNA production, it is possible to study viruses that behave similarly as a distinct group. Seven Baltimore groups are described that take into consideration whether the viral genome is made of deoxyribonucleic acid (DNA) or ribonucleic acid (RNA), whether the genome is single- or double-stranded, and whether the sense of a single-stranded RNA genome is positive or negative.
Amdoparvovirus is a genus of viruses in the family Parvoviridae in the subfamily Parvovirinae. Mustelids, skunk, and raccoons serve as natural hosts. There are five species in this genus. Diseases associated with this genus include progressive disorder of immune system.
Carnivore bocaparvovirus 1, formerly Canine minute virus is a species of Bocaparvovirus of the family Parvoviridae that infects dogs. It is similar to bovine parvovirus in its protein structure and DNA. A virus causing respiratory disease in humans has been called human bocavirus due to its similarity to these viruses. Canine minute virus was originally discovered in Germany in 1967 in military dogs, although it was originally thought to not cause disease. Dogs and puppies are infected orally, and the virus is spread transplacentally to the fetuses. Symptoms are seen most commonly between the ages of one to three weeks and include severe diarrhea, difficulty breathing, and anorexia. In severe cases, illness can be fatal.
Dependoparvovirus is a genus in the subfamily Parvovirinae of the virus family Parvoviridae; they are Group II viruses according to the Baltimore classification. Some dependoparvoviruses are also known as adeno-associated viruses because they cannot replicate productively in their host cell without the cell being coinfected by a helper virus such as an adenovirus, a herpesvirus, or a vaccinia virus.
Human bocavirus (HBoV) is the name given to all viruses in the genus Bocaparvovirus of virus family Parvoviridae that are known to infect humans. HBoV1 and HBoV3 are members of species Primate bocaparvovirus 1 whereas viruses HBoV2 and HBoV4 belong to species Primate bocaparvovirus 2. Some of these viruses cause human disease. HBoV1 is strongly implicated in causing some cases of lower respiratory tract infection, especially in young children, and several of the viruses have been linked to gastroenteritis, although the full clinical role of this emerging infectious disease remains to be elucidated.
Bocaparvovirus is a genus of viruses in the subfamily Parvovirinae of the virus family Parvoviridae. Humans, cattle, and dogs serve as natural hosts. There are 28 species in this genus. Diseases associated with this genus include, in humans, acute respiratory illness, and in cattle, diarrhea and mild respiratory symptoms.
Densovirinae is a subfamily of single-stranded DNA viruses in the family Parvoviridae. The subfamily has 11 recognized genera and 21 species. Densoviruses are known to infect members of insect orders Blattodea, Diptera, Hemiptera, Hymenoptera, Lepidoptera, and Orthoptera, while some viruses infect and multiply in crustaceans such as shrimp or crayfish, or sea stars from phylum Echinodermata.
Tetraparvovirus are a genus of viruses in the family Parvoviridae. There are six recognized species: Chiropteran tetraparvovirus 1, Primate tetraparvovirus 1, Ungulate tetraparvovirus 1, Ungulate tetraparvovirus 2, Ungulate tetraparvovirus 3, and Ungulate tetraparvovirus 4.
Bidensovirus is a genus of single stranded DNA viruses that infect invertebrates. The species in this genus were originally classified in the family Parvoviridae but were moved to a new genus because of significant differences in the genomes.
Self-complementary adeno-associated virus (scAAV) is a viral vector engineered from the naturally occurring adeno-associated virus (AAV) to be used as a tool for gene therapy. Use of recombinant AAV (rAAV) has been successful in clinical trials addressing a variety of diseases. This lab-made progeny of rAAV is termed "self-complementary" because the coding region has been designed to form an intra-molecular double-stranded DNA template. A rate-limiting step for the standard AAV genome involves the second-strand synthesis since the typical AAV genome is a single-stranded DNA template. However, this is not the case for scAAV genomes. Upon infection, rather than waiting for cell mediated synthesis of the second strand, the two complementary halves of scAAV will associate to form one double stranded DNA (dsDNA) unit that is ready for immediate replication and transcription. The caveat of this construct is that instead of the full coding capacity found in rAAV (4.7–6kb) scAAV can only hold about half of that amount (≈2.4kb).
Minute virus of mice (MVM) is the exemplar virus of the species Rodent protoparvovirus 1, in the genus Protoparvovirus of the Parvoviridae family of viruses. MVM exists in multiple variant forms including MVMp, which is the prototype strain that infects cells of fibroblast origin, while MVMi, the immunosuppressive strain, infects T lymphocytes. MVM is a common infection in laboratory mice due to its highly contagious nature. The virus can be shed from infected mice via feces and urine, but also via fomites and nasal secretions. Typically there are no clinical signs of infection in adult mice, however, experimental infection can cause multiple organ damage during fetal development or shortly after birth.
Protoparvovirus is a genus of viruses in the Parvovirinae subfamily of the virus family Parvoviridae. Vertebrates serve as natural hosts. There are 15 species in the genus including Rodent protoparvovirus 1 for which the exemplar virus is minute virus of mice (MVM). This genus also includes canine parvovirus (CPV), which causes gastrointestinal tract damage in puppies that is about 80% fatal, and porcine parvovirus (PPV), which is a major cause of fetal death and infertility in pigs. The genus divides phylogenetically into two branches, one that contains many founder members of the family, such as MVM, CPV and PPV, which have been studied in considerable detail, and a second branch occupied exclusively by predicted viruses whose coding sequences were identified recently in the wild using virus discovery approaches, but whose biology remains minimally explored. This second branch currently contains two species whose members infect humans, called Primate protoparvovirus 1 and Primate protoparvovirus 3. Until 2014, the genus was called Parvovirus, but it was renamed to eliminate confusion between members of this genus and members of the entire family Parvoviridae.
Aveparvovirus is a genus of viruses, in the subfamily Parvovirinae of the virus family Parvoviridae. There are three species in this genus. Diseases associated with this genus include: enteric disease and malabsorption syndrome.
Spiraviridae is a family of incertae sedis viruses that replicate in hyperthermophilic archaea of the genus Aeropyrum, specifically Aeropyrum pernix. The family contains one genus, Alphaspiravirus, which contains one species, Aeropyrum coil-shaped virus. The virions of ACV are non-enveloped and in the shape of hollow cylinders that are formed by a coiling fiber that consists of two intertwining halves of the circular DNA strand inside a capsid. An appendage protrudes from each end of the cylindrical virion. The viral genome is ssDNA(+) and encodes for significantly more genes than other known ssDNA viruses. ACV is also unique in that it appears to lack its own enzymes to aid replication, instead likely using the host cell's replisomes. ACV has no known relation to any other archaea-infecting viruses, but it does share its coil-like morphology with some other archaeal viruses, suggesting that such viruses may be an ancient lineage that only infect archaea.
Monodnaviria is a realm of viruses that includes all single-stranded DNA viruses that encode an endonuclease of the HUH superfamily that initiates rolling circle replication of the circular viral genome. Viruses descended from such viruses are also included in the realm, including certain linear single-stranded DNA (ssDNA) viruses and circular double-stranded DNA (dsDNA) viruses. These atypical members typically replicate through means other than rolling circle replication.
Rolling hairpin replication (RHR) is a unidirectional, strand displacement form of DNA replication used by parvoviruses, a group of viruses that constitute the family Parvoviridae. Parvoviruses have linear, single-stranded DNA (ssDNA) genomes in which the coding portion of the genome is flanked by telomeres at each end that form hairpin loops. During RHR, these hairpin loops repeatedly unfold and refold to change the direction of DNA replication so that replication progresses in a continuous manner back and forth across the genome. RHR is initiated and terminated by an endonuclease encoded by parvoviruses that is variously called NS1 or Rep, and RHR is similar to rolling circle replication, which is used by ssDNA viruses that have circular genomes.
This page is based on this Wikipedia article Text is available under the CC BY-SA 4.0 license; additional terms may apply. Images, videos and audio are available under their respective licenses.
