Satellites:
As far as satellites go, they can be divided into two main categories: those that encode their own coat protein, and those that do not. To simplify, one example will be chosen to be a representation of each group. Satellite tobacco necrosis virus will represent the group of satellites that encode their own coat protein because it is the most studied. Hepatitis delta virus will represent the group of satellites that do not encode their own protein, because it is the only known satellite to infect human cells (thus making it a lot more interesting than all the plant satellites!). (Matthews, 1992).
Satellite tobacco necrosis virus life cycle and transmission:
[ UCSF Computer Graphics Laboratory. Virus Capsid Images http://www.cgl.ucsf.edu/Research/virus/capsids/viruses.html, accessed April 11, 2011. ]
Above is a picture of satellite tobacco necrosis virus (STNV). Its helper virus is tobacco necrosis virus, which is a small icosohedral virus. Only certain strains of the helper virus are able to activate the satellite virus. Both are found to infect plant roots.
Little is known about the exact mechanisms of the STNV life cycle, but here’s what we do know: it has a ssRNA genome that is not similar to the helper virus genome. STNV is very stable in vivo, and has been shown to survive in leaves for ten days without the helper virus. This implies that, after uncoating, the STNV is able to essentially wait for a period of time for helper virus to infect the cell and aid with its replication (remember, satellites are completely dependent on helper viruses for replication of their RNA). Once helper virus infection occurs, the satellite virus is able to replicate. The amino acid sequence of STNV has been determined, and it codes for just one product: its coat protein. Replication occurs in the cytoplasm from the satellite’s own RNA transcript. (Matthews, 1992) (Voyles, 1993).
A bit more is known about the transmission of STNV. There have been four factors named that play a role in transmission of STNV: the strains of the satellite and helper viruses, type of fungus, and species of host plant. STNV, as well as its helper virus, are primarily transmitted by the fungus Olpidium brassicae. This fungus serves as a vector for transmission of STNV, as it rests in the soil. Its spores release the virus into the soil from infected plant root cells, which can then be absorbed by other nearby plant root cells. (Matthews, 1992).
Sources:
Matthews, R.E.F. Fundamentals of Plant Virology. San Diego: Academic Press, Inc., 1992.
Voyles, Bruce. The Biology of Viruses. St. Louis: Mosby-Year Book, Inc., 1993.
Hepatitis delta virus life cycle and transmission:
[Ashton, Eric. Feb 2000. Hepatitis Delta Virus http://www.stanford.edu/group/virus/delta/2000/deltaagent.html, retrieved April 11, 2011.]
Above is a picture of hepatitis delta virus (HDV). This virus is a satellite of hepatitis B virus. Although it has characteristics similar to viroids, it is typically considered a satellite.
Again, specific mechanisms of the life cycle are not always clear, but it is obvious that HDV infects the same cells (liver) as hepatitis B virus because it needs the helper for replication. It has a lipid coat plus hepatitis B antigens on its surface. HDV has a circular RNA genome containing its own “delta antigen”, and circulates through the blood. It is not known exactly how HDV enters liver cells, but one hypothesis is that interaction occurs between the hepatitis B surface antigen on HDV and a host cellular receptor. After HDV enters the cell, replication occurs, and at this point, does not need assistance from the helper hepatitis B virus as it utilizes all host cell machinery. After replication, post-translation editing of the RNA takes place so that two slightly different forms of the delta protein emerge. One form is responsible for aiding further HDV replication; the other is necessary for assembly and release of HDV viral particles. Infection with the helper virus is necessary for assembly of HDV particles, and is thought to occur only with an initiating interaction between hepatitis B antigen (from the helper virus) and HDV antigen. The envelope proteins are provided by hepatitis B, which is why HDV is representative of a satellite that does not encode its own coat proteins. HDV exits the cell through the Golgi apparatus. Here it acquires the hepatitis B antigen proteins on its surface.(Maramorosch, 1991).
Transmission of HDV occurs in much the same way of other types of hepatitis: it can be sexually transmitted, or through contact with infected blood (IV drug use, tattoos, etc). (WHO, 2001).
Sources:
Maramorosch, Karl. Viroids and Satellites: Molecular Parasites at the Frontier of Life. Boca Raton: CRC Press, 1991.
World Health Organization. 2001. Hepatitis Delta. http://www.who.int/csr/disease/hepatitis/HepatitisD_whocdscsrncs2001_1.pdf, retrieved April 11, 2011.
Viroids:
Viroids can infect plant only through mechanical break in the plant (ex: insect), which is the way they enter the host. They enter the organelle (chloroplast or nucleus) and replicate in there. The next step is viral movement through plasmodesmota (cell-to-cell movement) and/or the phloem (systemic movement) (3). There is no information on a specific “life cycle” for viroids.
This is an image of systemic infection of both type species PSTVd and ASBVd (4).
Viroids are mainly transmitted through vegetative propagation, which is asexual reproduction where the daughter plant is exactly the same as the host plant. They can also be transmitted through equipment, pollen and plant to plant movement in a windy weather for example (5). The main insects that infect plants are aphids and grasshoppers. Nematode larvae could also infect plants by eating from it. Pollen is another way of spreading the viroids (6).
Satellites and Viroids 
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