Plectrovirus

Plectrovirus
Virus classification
Group: Group II (ssDNA)
Family: Inoviridae
Genus: Plectrovirus
Type Species
  • Acholeplasma phage MV-L51

Plectrovirus is a genus of viruses, in the family Inoviridae. Bacteria in the phylum Tenericutes serve as natural hosts, making these viruses bacteriophages. There are currently seven species in this genus including the type species Acholeplasma phage MV-L51.[1][2]

Taxonomy

Group: ssDNA

[2]

Virology

The virons are non-enveloped, rod-shaped and filamentous. The capsid has a helical symmetry and is generally has a length of 85–280 nm or 760–1950 nm and a width of 10–16 nm or 6–8 nm respectively. These morphological differences depend on the species.[3]

There are five or more proteins in the capid: gp8 (the major capsid protein); gp6, gp7 and gp8 (minor capsid proteins); and gp3, which acts as the initial host binding protein.[3]

The genomes are non-segmented, circular, positive-sense, single-stranded DNA 4.4–8.5 kilobases in length. They encode 4 to 11 proteins. Replication of the genome occurs via a dsDNA intermediate and the rolling circle mechanism. Gene transcription is by the host's cellular machinery each gene having a specific promoter.[3]

Genus Structure Symmetry Capsid Genomic Arrangement Genomic Segmentation
PlectrovirusRod-shapedNon-EnvelopedCircularMonopartite

Life cycle

There are six steps in the life cycle

1. Adsorption to the host via specific receptor(s)

2. Movement of the viral DNA into the host cell

3. Conversion of the single strand form to a double stranded intermediate

4. Replication of the viral genome

5. Synthesis of the new virons

6. Release of the new virons from the host

A typical replication cycle normally take 10–15 minutes to complete.[3]

Genus Host Details Tissue Tropism Entry Details Release Details Replication Site Assembly Site Transmission
PlectrovirusBacteriaNonePilus adsorptionSecretionCytoplasmCytoplasmPilus

Adsorption

This is mediated by one of the viral proteins (gp3) binding to the host receptor.[3]

Conversion to double stranded form

The conversion from single-stranded to double-stranded form is carried out by the host's own DNA polymerase. The host's RNA polymerase binds to the viral genome and syntheses RNA. Some of this RNA is translated and the remainder is used to initiate DNA replication.[3]

Replication

This is initiated when a viral endonuclease (gp2) nicks the double stranded intermediate. This nicking site is specific and the sequence around the site highly symmetrical. The activity of gp2 is regulated by two other viral proteins: gp5 (single strand binding protein) and gp10. New viral genomes are produced via the rolling circle mechanism. These new single strand DNA sequences become templates for further DNA and RNA synthesis. When sufficient gp5 has accumulated within the cell, further DNA synthesis is halted and viron assembly begins.[3]

Viron assembly

This is a complex process. It is initiated by the formation of a complex of gp1, gp7, gp9 and gp11 along with the single stranded DNA and gp%. It begins at a specific sequence within the DNA which is predicted to have a hairpin formation. Assembly continues at the membrane where ~1500 subunits of gp5 are displaced by ~2700 subunits of gp8 (the number of major capid protein subunits per viron). This process involves both gp1 and gp11. Assembly is completed by the addition of the viral proteins gp3 and gp6. In hosts with both an inner and outer membrane adhesion zones are created by gp4, a process that may also involve gp1.[3]

Viron release

Typically productive infection occurs by budding from the host membrane without lysis of the host.[3]

Notes

A number of exceptions to this life cycle are known. Lysogenic species, which encode integrases, exist within this family.[3]

References

  1. ↑ "Viral Zone". ExPASy. Retrieved 15 June 2015.
  2. 1 2 ICTV. "Virus Taxonomy: 2014 Release". Retrieved 15 June 2015.
  3. 1 2 3 4 5 6 7 8 9 10 Melcher U, Comer J. 2011. Plectrovirus. In: The Springer Index of Viruses. Tidona, C & Darai, G, editors. Springer New York pp. 749–755. doi:10.1007/978-0-387-95919-1_106
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