What’s the Difference Between Parvoviruses and Other ssDNA Viruses?

Parvoviruses and other single-stranded DNA (ssDNA) viruses are tiny but powerful pathogens that can affect a wide range of living organisms. Despite their small size, these viruses can lead to serious health issues in animals and humans alike. In this post, we will explore what parvoviruses are, how they differ from other viruses, and their impact on health and disease. We will also discuss the importance of understanding these unique viruses in the fields of medicine and science.

With virions ranging in diameter from 18 to 26 nm, parvoviruses are among the tiniest viruses currently known to science. The Latin word parvus, which means little, is where they got their name. The Parvoviridae family is divided into two subfamilies: Parvovirinae (vertebrate viruses) and Densovirinae (invertebrate viruses).

The subfamily Parvovirinae comprises the genus Dependovirus, whose members are defective and often only replicate when a helper virus co-infects the cell. Other parvoviruses as autonomous parvoviruses since they do not require helper viruses.

Table 1 some of the viruses in the family Parvoviridae

Structure of Parvovirus

Virion

Parvoviruses are small, simple viruses with a simple ssDNA genome enclosed within an icosahedral symmetry capsid.

The Capsid

The parvovirus capsid is composed of 60 protein molecules, with one species forming the majority. The capsid structure is numbered in size, with VP1 being the largest. Smaller proteins are shorter versions of VP1. Each protein species has an eight-stranded β-barrel structure, a common feature in viral capsid proteins, including those of picornaviruses.

The virion is a spherical structure with surface protrusions and canyons, with a central protrusion at each vertices of the icosahedron.

The Genome

Parvoviruses have genomes of linear ssDNA ranging from 4-6 kb, with short complementary sequences at each end that form a secondary structure. Some parvoviruses have inverted terminal repeats (ITRs), where one end is complementary to the other, resulting in identical secondary structures. However, other parvoviruses have unique sequences at each end of the DNA, resulting in a unique secondary structure.

The genes for non-structural proteins are located at the 3rd end of (−) DNA, while those for structural proteins are located at the 5th end.

Table 2 Percentages of parvovirus virions containing (+) and (−) strand DNA

Parvovirus replication

Parvoviruses have a small genome with only a few proteins, relying on host cells or another viruses for important proteins. These proteins, such as DNA polymerase and DNA replication proteins, are only available during the S phase of the cell cycle, limiting replication opportunities. This contrasts with large DNA viruses like herpes viruses, which have their own DNA-replicating enzymes, allowing replication in any phase of the cell cycle.

Attachment and entry

A virion attaches to receptors on the surface of a potential host cell, such as a red blood cell precursor, and the blood group P antigen in B19 virus. The virion enters the cell via endocytosis and is released into the cytoplasm, where it associates with microtubules and is transported to a nuclear pore. The parvovirus virion, with a diameter of 18-26 nm, can pass through a nuclear pore, but it must undergo structural changes before entering the nucleus.

Single-stranded DNA to double-stranded DNA

The virus genome is converted into dsDNA in the nucleus by a cell DNA polymerase, with the ends double-stranded due to base pairing and the –OH group at the 3′ end acting as a primer.

Transcription and translation

Cell RNA polymerase II transcribes virus genes, with cell transcription factors playing crucial roles. Primary transcripts undergo splicing events to produce two mRNA classes: larger mRNAs encode non-structural proteins, and smaller mRNAs encode structural proteins.

Non-structural proteins are phosphorylated and play a crucial role in gene expression and DNA replication.

DNA replication

The virion assembly converts the ssDNA genome to dsDNA, which is then replicated using rolling-hairpin replication, a leading strand mechanism, distinguishing parvoviruses from other DNA viruses that replicate their genomes through leading and lagging strand synthesis.

Procapsids are made from structural proteins and filled with a virus genome copy, either (+) or (-) DNA. A non-structural protein acts as a helicase, unwinding the dsDNA for a single strand to enter the procapsid.

1. Attachment 2. Entry 3. Transcription 4. Translation 5. Genome replication 6. Assembly 7. Exit

Dependovirus replication

A cell can be productively infected with both a dependovirus and an appropriate helper virus when co-infected.

Dependoviruses often infect cells without a helper virus, integrating their genome into a cell chromosome through recombination. This results in a latent infection, which can occur in human and monkey cell lines. In humans, the virus DNA is integrated at a specific site on chromosome 19. If a cell with a latent dependoviral genome becomes infected with an appropriate helper virus, a productive infection with both viruses can occur.

Other ssDNA viruses

Table below provides examples of viruses with ssDNA genomes, most of which have circular genomes.

Common Examples of parvoviruses

Dependoviruses

The first dependovirus to be identified was found in an adenovirus preparation under an electron microscope. It was discovered that the contamination was a satellite virus, a faulty virus that needs the adenovirus’s assistance to replicate. As a result, the satellite virus was given the name “adeno-associated virus.” Since then, other serotypes of dependoviruses have been discovered in adenovirus preparations, infected people, and other species.
According to survey results obtained using serological techniques and PCR identification of virus DNA, dependovirus infections are common.

Not every dependovirus needs an adenovirus to be completely successful. In rare situations, dependoviruses can replicate in the absence of a helper virus, and other DNA viruses, such as herpesviruses, can occasionally serve as helpers.

Dependoviruses are valuable gene vectors used for mass production of proteins in cell cultures, and are being investigated for treating genetic diseases and cancers due to their lack of known disease causes compared to retroviruses.

Autonomous parvoviruses

In serum from a healthy blood donor, a parvovirus that doesn’t need a helper virus was found. Red blood cell precursors are infected by the virus, which bears the designation B19 after a batch of blood. While the majority of B19 infections are asymptomatic, some can lead to illness, such as erythema infectiosum, or fifth disease, which causes youngsters to appear “slapped on the cheek”.

B19 virus can cause acute arthritis, aplastic anaemia in chronic haemolytic anaemia, and hydrops foetalis, which can be passed from a pregnant mother to the fetus and lead to death.

In 2005, a new human parvovirus was discovered through molecular screening of nasopharyngeal aspirates from children with lower respiratory tract disease, related to known Bocaviruses.

Viruses belonging to the Densovirinae subfamily induce dense inclusions to develop in the infected cell’s nucleus. Certain viruses can lead to financial harm to the silk industry as they are diseases of the silkworm, or Bombyx mori.

In summary, parvoviruses and other single-stranded DNA (ssDNA) viruses play crucial roles in both wildlife and human health. Their unique structures and ability to infect host cells offer valuable insights into viral behavior and disease management. Understanding these viruses can lead to better treatments and preventive measures. Stay informed about the latest research in virology to appreciate the complexity and importance of these tiny but mighty pathogens. Knowledge is your best defense.

Source: VIROLOGY PRINCIPLES AND APPLICATIONS, John B. Carter and Venetia A. Saunders