Plectrovirus

Plectrovirus is a genus of viruses, in the family Plectroviridae. Bacteria in the phylum Tenericutes serve as natural hosts, making these viruses bacteriophages. The type species Acholeplasma virus L51 is the only recognized species in the genus.[1][2]

Plectrovirus
Virus classification
(unranked): Virus
Realm: Monodnaviria
Kingdom: Loebvirae
Phylum: Hofneiviricota
Class: Faserviricetes
Order: Tubulavirales
Family: Plectroviridae
Genus: Plectrovirus
Type species
Acholeplasma virus L51

Virology

The virons are non-enveloped and rod-shaped. 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]

GenusStructureSymmetryCapsidGenomic arrangementGenomic 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]

GenusHost detailsTissue tropismEntry detailsRelease detailsReplication siteAssembly siteTransmission
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 gp1# 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 gp1# 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. ICTV. "Virus Taxonomy: 2019 Release". Retrieved 4 July 2020.
  3. 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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