The abnormal form is called PrP sc for scrapie-associated prion protein , and the normal cellular form is called PrP c. Evidence supports a model in which entry of PrP sc into the brain of an animal causes the PrP c protein to change from its normal conformation to the abnormal form. How the PrP sc causes this conformational change is unclear.
However, the best-supported model is that the PrP sc directly interacts with PrP c , causing the change. It is noteworthy that mice lacking the PrP gene cannot be infected with PrP sc.
Although evidence is strong that PrP sc causes PrP c 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 PrP c is anchored to the plasma membrane. Its conversion to PrP sc and subsequent aggregation may interfere with membrane functions. Nonetheless, the subsequent pointers compare viruses against viroids and prions, respectively. Both are infectious agents made of genetic material. Similar to a virus, a viroid lacks energy and metabolic mechanisms. It also depends on a host to replicate and evolve. Below are the key differences viroids from viruses:.
They do not code for any protein. The smallest known viruses are around nucleobases long. Viroids do not have one. When this normal protein becomes a prion, it becomes dangerous and can cause several mostly fatal neurodegenerative brain diseases. The most well-known disease caused by prions is mad cow disease the human form is Creutzfeldt-Jakob disease.
Once prions enter the brain, they force the normal cellular proteins to begin folding into abnormal shapes. This destroys the neurons and eventually leads the brain to become riddled with holes. This spongelike brain consistency is where the medical name for mad cow disease comes from — bovine spongiform encephalopathy BSE. Prions also cause the condition "scrapie," a degenerative disease affecting the nervous system, in sheep and goats. Prions can cause a few human diseases, although they're extremely rare.
One disease, kuru , is associated with cannibalism. Some scientists believe that prions may also have a role in Alzheimer's disease [source: Microbe World ]. There is no treatment for any prion-caused disease. Unlike viruses, viroids do not have a protein coat to protect their genetic information. Viroids can result in devastating losses of commercially important agricultural food crops grown in fields and orchards. Since the discovery of PSTV, other viroids have been discovered that cause diseases in plants.
Tomato planta macho viroid TPMVd infects tomato plants, which causes loss of chlorophyll, disfigured and brittle leaves, and very small tomatoes, resulting in loss of productivity in this field crop. Avocado sunblotch viroid ASBVd results in lower yields and poorer-quality fruit. ASBVd is the smallest viroid discovered thus far that infects plants. Peach latent mosaic viroid PLMVd can cause necrosis of flower buds and branches, and wounding of ripened fruit, which leads to fungal and bacterial growth in the fruit.
PLMVd can also cause similar pathological changes in plums, nectarines, apricots, and cherries, resulting in decreased productivity in these orchards, as well. Viroids, in general, can be dispersed mechanically during crop maintenance or harvesting, vegetative reproduction, and possibly via seeds and insects, resulting in a severe drop in food availability and devastating economic consequences.
A second type of pathogenic RNA that can infect commercially important agricultural crops are the virusoid s , which are subviral particles best described as non—self-replicating ssRNAs. There are currently only five described types of virusoids and their associated helper viruses. The helper viruses are all from the family of Sobemoviruses. An example of a helper virus is the subterranean clover mottle virus, which has an associated virusoid packaged inside the viral capsid. Once the helper virus enters the host cell, the virusoids are released and can be found free in plant cell cytoplasm, where they possess ribozyme activity.
The helper virus undergoes typical viral replication independent of the activity of the virusoid. The virusoid genomes are small, only to nucleotides long. A virusoid genome does not code for any proteins, but instead serves only to replicate virusoid RNA.
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