6.4: Viroids, virusoids and prions (2023)

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    Learning Objectives
    • Describe viroids and their unique properties
    • Describe virusoids and their unique properties
    • Describe prions and their unique properties

    Research efforts to discover the causes of previously unresearched diseases have led to the discovery of non-living pathogens that are very different from viruses. These include RNA-only or protein-only particles that are nevertheless able to reproduce themselves at the expense of a host—an important similarity to viruses that enables them to cause disease. To date, these discoveries include viroids, viroids, and proteinaceous prions.


    In 1971, Theodor Diener, a pathologist working at the Agriculture Research Service, discovered an acellular particle he called a viroid, meaning "virus-like". Viroids consist of only a short strand of circular RNA capable of self-replication. The first viroid discovered was found to be the cause of potato tuber disease, which germinates more slowly and causes various malformations in potato plants (see Figure \(\PageIndex{1}\)). Like viruses, potato spindle tuber viroids (PSTVs) take control of the host machinery to replicate their RNA genome. Unlike viruses, viroids do not have a protein coat to protect their genetic information.

    6.4: Viroids, virusoids and prions (2)

    Viroids can lead to devastating losses of commercially important agricultural crops grown in fields and orchards. Since the discovery of PSTV, other viroids have been discovered to cause disease in plants. Tomato planta macho viroid (TPMVd) infects tomato plants, leading to loss of chlorophyll, deformed 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 lower quality fruit. ASBVd is the smallest viroid discovered to date that infects plants. Peach latent mosaic viroid (PLMVd) can cause necrosis of flower buds and branches and damage to ripening fruit, leading to fungal and bacterial growth in the fruit. PLMVd can also cause similar pathological changes in plums, nectarines, apricots and cherries, resulting in reduced productivity in these orchards. Viroids can generally be spread mechanically during crop maintenance or harvesting, vegetative reproduction, and possibly via seeds and insects, resulting in a severe decrease in food availability and devastating economic consequences.


    Another type of pathogenic RNA that can infect commercially important agricultural crops is the viroids, which are subviral particles best described as non-self-replicating ssRNAs. RNA replication of viroids is similar to that of viroids, but unlike viroids, viroids require the cell to also be infected with a specific "helper" virus. There are currently only five described types of virusoids and their associated helper viruses. The helper viruses all come from the family of Sobemoviruses. An example of a helper virus is the subterranean shamrock broge virus, which has an associated virusoid packaged in the viral capsid. Once the helper virus enters the host cell, the viroids are released and can be found freely in the cytoplasm of plant cells, where they have ribozyme activity. The helper virus typically undergoes viral replication independently of virusoid activity. The virusoid genomes are small, only 220 to 388 nucleotides long. A virusoid genome does not code for proteins, but instead serves only to replicate virusoid RNA.

    Virusoids belong to a larger group of infectious agents called satellite RNAs. These are similar pathogenic RNAs found in animals. Unlike the plant viroids, satellite RNAs can code for proteins; however, like plant viroids, satellite RNAs must co-infect with a helper virus to replicate. One satellite RNA that infects humans and has been described as a virus by some scientists is hepatitis delta virus (HDV), which some reports also call hepatitis delta virus. HDV is much larger than a plant virus, has a circular ssRNA genome of 1700 nucleotides, and can direct the biosynthesis of HDV-associated proteins. HDV helper virus is hepatitis B virus (HBV). Co-infection with HBV and HDV results in more severe pathological changes in the liver during infection, which is how HDV was first discovered.

    Exercise \(\PageIndex{2}\)

    What is the main difference between a viroid and a virusoid?


    Scientists once believed that any infectious particle must contain DNA or RNA. Then, in 1982, Stanley Prusiner, a physician studying scrapie (a fatal, degenerative disease of sheep), discovered that the disease was caused by proteinaceous infectious particles, or prions. Because proteins are acellular and do not contain DNA or RNA, Prusiner's findings were initially met with resistance and skepticism; however, his research was eventually validated and he was awarded the 1997 Nobel Prize in Physiology or Medicine.

    6.4: Viroids, virusoids and prions (3)

    A prion is a misfolded rogue form of a normal protein (PrPc) found in the cell. This rogue prion protein (PrPsc), which can be caused by a genetic mutation or arise spontaneously, can be infectious and stimulate other endogenous normal proteins to misfold and form plaques (see image \(\PageIndex{2}\)) . It is now known that prions can cause various forms of transmissible spongiform encephalopathy (TSE) in humans and animals. TSE is a rare degenerative disease that affects the brain and nervous system. The build-up of junk proteins causes the brain tissue to mushroom, killing brain cells and creating holes in the tissue, leading to brain damage, loss of motor coordination and dementia (see image \(\PageIndex{3}\)) . Infected individuals are mentally disabled and unable to move or speak. There is no cure and the disease progresses rapidly, ultimately leading to death within months or years.

    6.4: Viroids, virusoids and prions (4)

    TSEs in humans are kuru, fatal familial insomnia, Gerstmann-Straussler-Scheinker disease, and Creutzfeldt-Jakob disease (see Figure \(\PageIndex{3}\)). Animal TSEs include mad cow disease, scrapie (in sheep and goats) and chronic wasting disease (in moose and deer). TSEs can be transmitted between animals and from animals to humans by eating contaminated meat or feed. Human-to-human transmission can occur through heredity (as is often the case with GSS and CJD) or through contact with infected tissue, as can occur during a blood transfusion or organ transplant. There is no evidence of transmission through casual contact with an infected person. Table \(\PageIndex{1}\) provides an overview of TSEs affecting humans and their mode of transmission.

    Prions are extremely difficult to destroy because they are resistant to heat, chemicals and radiation. Even standard sterilization procedures do not guarantee the destruction of these particles. Currently, there is no treatment or cure for TSE disease, and contaminated meat or animals must be handled according to federal guidelines to prevent transmission.

    Table \(\PageIndex{1}\): Transmissible spongiform encephalopathies (TSEs) in humans
    Disease Transfer mechanism(s).1
    Sporadic CJD (sCJD) Unknown; possibly due to alteration of normal precursor protein (PrP) to rogue state due to somatic mutation
    Variant CJD (vCJD) Eating contaminated livestock products and by secondary transmission through blood
    Family CJD (fCJD) Mutation i kimlinje PrP-gen
    Iatrogen CJD (iCJD) Contaminated neurosurgical instruments, corneal graft, gonadotrophic hormone and secondary to blood transfusion
    Which one Eating infected flesh through ritual cannibalism
    Gerstmann-Straussler-Scheinkers sygdom (GSS) Mutation i kimlinje PrP-gen
    Fatal Familial Insomnia (FFI) Mutation i kimlinje PrP-gen
    Exercise \(\PageIndex{3}\)

    Does a prion have a genome?

    For more information on handling animals and materials contaminated with prions, refer to the guidelines published on the CDC and WHO websites.

    Clinical focus: resolution

    A few days later, David's doctor receives the results of the immunofluorescence test on his skin sample. The test is negative for the rabies antigen. Another viral antigen test on his saliva sample is also negative. Despite these results, the doctor decides to continue David's current treatment. Given the positive RT-PCR test, it is best not to rule out a possible rabies infection.

    Near the bite site, David receives an injection of rabies immune globulin, which binds to and inactivates any rabies virus that may be present in his tissues. Over the next 14 days, he will receive a series of four rabies-specific vaccinations in his arm. These vaccines activate David's immune response and help his body recognize and fight the virus. Fortunately, David's symptoms improve with treatment and he makes a full recovery.

    Not all cases of rabies have such a happy ending. In fact, rabies is usually fatal by the time the patient begins to show symptoms, and post-bite treatments are primarily palliative (ie, sedation and pain management).


    • Other acellular agents such asviral,vira, iprioneralso cause disease. Viroids consist of small, naked ssRNAs that cause disease in plants. Virusoids are ssRNAs that other helper viruses require to establish an infection. Prions are proteinaceous infectious particles thattransmissible spongiform encephalopathies.
    • Prions are extremely resistant to chemicals, heat and radiation.
    • There are no treatments for prion infection.


    1. National Institute of Neurological Disorders and Stroke. "Creutzfeldt-Jakob Disease Fact Sheet."http://www.ninds.nih.gov/disorders/cjd/detail_cjd.htm(accessed 31 December 2015).


    • Nina Parker, (Shenandoah University), Mark Schneegurt (Wichita State University), Anh-Hue Thi Tu (Georgia Southwestern State University), Philip Lister (Central New Mexico Community College) and Brian M. Forster (Saint Joseph's University) with many contributors authors. Original content via Openstax (CC BY 4.0; free access athttps://openstax.org/books/microbiology/pages/1-introduction)


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