||This article may be too technical for most readers to understand. (September 2011)|
|Group:||Group II (ssDNA)|
The virions are non-enveloped, rod-shaped and filamentous. The capsid has a helical symmetry and in general 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.
There are five or more proteins in the capsid: gp8 (the major capsid protein); gp6, gp7, and gp8 (minor capsid proteins); and gp3, which acts as the initial host-binding protein.
The viral 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.
There are six steps in the life cycle
- Adsorbion to the host via specific receptor(s)
- Movement of the viral DNA into the host cell
- Conversion of the single strand form to a double-stranded intermediate
- Replication of the viral genome
- Synthesis of the new virons
- Release of the new virons from the host
A typical replication cycle normally take 10–15 minutes to complete.
This is mediated by one of the viral proteins (gp3) binding to the host receptor
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.
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.
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 that 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.
This may involve host lysis but alternatively productive infection may occur by budding from the host membrane. This pattern is typically seen in the Plectivirus genus.
A number of exceptions to this life cycle are known. Lysogenic species, which encode integrases, exist within this family.
There are two genera in this family: Inovirus and Plectrovirus. These genera differ in their host range: The species in the Plectrovirus genus infect hosts of the class Mollicutes while those of the genus Inovirus infect species of Enterobacteriaceae, Pseudomonadaceae, Spirillaceae, Xanthomonadaceae, Clostridium and Propionibacterium.