Overview of Viroids, Satellites and prions

Viroids, Satellites and prions


Viruses are simple, Viroids are infectious agents that consist only of RNA. They cause over 20 different plant diseases, including potato spindle-tuber disease, exocortis disease of citrus trees, and chrysanthemum stunt disease. Viroids are covalently closed, circular ssRNAs, about 250 to 370 nucleotides long.

The circular RNA exists as a rodlike shape due to intrastrand base pairing, which forms double-stranded regions with singlestranded loops. Some viroids are found in the nucleolus of infected host cells, where between 200 and l 0,000 copies may be present. Others are located within chloroplasts.

Viroid Structure
This schematic diagram shows the general organization of a viroid. The closed single-stranded RNA circle has extensive intrastrand base pairing and interspersed unpaired loops. Viroids have five domains. Most changes in viroid pathogenicity arise from variations in the P and TL domains.

The RNA of viroids does not encode any gene products, so they cannot replicate themselves. Rather, evidence exists that a viroid is replicated by a host cell enzyme called a DNA-dependent RNA polymerase. This enzyme normally functions in the host to synthesize RNA using DNA as the template during transcription.

However, when infected by a viroid, the host polymerase evidently uses the viroid RNA as a template for RNA synthesis, rather than its own DNA. The host polymerase synthesizes a complementary RNA molecule, which then serves as the template for synthesis of new viroid RNAs.

A plant may be infected with a viroid without showing symptoms; that is, it may have a latent infection. However, the same viroid in another host species may cause severe disease. The pathogenicity of viroids is not well understood, but it is known that particular regions of the RNA are required; studies have shown that removing these regions blocks the development of disease.

Some data suggest that viroids cause disease by triggering a eukaryotic response called RNA silencing, which normally functions to protect against infection by dsRNA viruses. During RNA silencing, the cell detects the presence of dsRNA and selectively degrades it.

Viroids may take over this response by hybridizing to specific host mRNA molecules to which they have a complementary nucleotide sequence. Formation of the viroid-host hybrid dsRNA molecule is thought to elicit RNA silencing. This results in destruction of the host mRNA and therefore silencing of the host gene. Failure to express a required host gene leads to disease in the host plant.


Satellites are similar to viroids in that they also consist only of a nucleic acid (either DNA or RNA). They differ from viroids in that they may encode one or more gene products and need ahelper virus to replicate and infect host cells. There is no homology between the genome of the satellite and its helper virus.

Satellites are further divided into three types: Satellite viruses, Satellite RNAs, and Satellite DNAs. Satellite viruses encode their own capsid proteins, whereas satellite RNAs and DNAs do not. Most satellites use plant viruses as their helper viruses.


Prions (proteinaceous infectious particle) cause a variety of neuro degenerative diseases in humans and other animals, including scrapie in sheep, bovine spongiform encephalopathy (BSE or “mad cow disease”) and the human diseases kuru, fatal familial insomnia, Creutzfeldt-Jakob disease (CJD), and  Gerstmann-Strassler-Scheinker syndrome (GSS). All result in progressive degeneration of the brain and eventual death. At present, no effective treatment exists.

The best-studied prion is the scrapie prion. Researchers have shown that scrapie is caused by an abnormal form of a cellular protein. The abnormal form is called PrPsc (for scrapie-associated prion protein), and the normal cellular form is called PrPc.

One Proposed Model for Prion Replication
Normal and prion proteins differ in their tertiary structures

Evidence supports a model in which entry of PrPsc into the brain of an animal causes the PrPc protein to change from its normal conformation to the abnormal form. The newly produced PrPsc molecules then convert more PrPc molecules into the abnormal PrPsc form. How the PrPsc causes this conformational change is unclear.

However, the best-supported model is that the PrPsc directly interacts with PrPc, causing the change. It is noteworthy that mice lacking the PrP gene cannot be infected with PrPsc.

Although evidence is strong that PrPsc causes PrPc to fold abnormally, how this triggers neuron loss is poorly understood. Some possible mechanisms include changes in plasma membrane structure of infected cells. It is known that PrPc is anchored to the plasma membrane. Its conversion to PrPsc and subsequent aggregation may interfere with membrane functions.

There is also evidence that both forms of PrP must be present in the cell for neuron death. It may be that an interaction between the two inhibits normal PrPc. As yet, the function of PrPc is unknown. However, evidence points to it having a protective role that prevents a cell from killing itself by a process called apoptosis (programmed cell death).

Reference and Sources

  • https://quizlet.com/170615486/prescott-microbiology-chapter-6-viruses-final-flash-cards/
  • https://www.coursehero.com/file/p5dj46l/Discuss-the-ways-that-viruses-can-be-cultivated-Define-the-termsplaque/
  • https://www.biologydiscussion.com/viruses/viral-agents-that-causes-diseases/50029
  • https://quizlet.com/149231652/prescott-microbiology-chapter-6-flash-cards/
  • https://www.brainscape.com/flashcards/lecture-4-viruses-and-other-acellular-inf-4732172/packs/6971492
  • https://www.scientificamerican.com/article/what-is-a-prion-specifica/
  • https://www.sciencedirect.com/topics/neuroscience/viroids
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC506947/
  • https://www.sciencedirect.com/topics/immunology-and-microbiology/helper-virus

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