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How do viroids propagate to other hosts?

How do viroids propagate to other hosts?


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As viroids are simply non-encapsidated non-coding RNA molecules, it is difficult to imagine a mechanism for their continual infection, other than horizontal transfer which doesn't seem to be the case.

Is there a working theory on how viroids propagate and continually infect hosts?


Viroids are commonly thought of as remnants from the "RNA world" since they are composed of only RNA and have ribozyme activity. Viroids can be considered as plant parasites of the transcriptional machinery of the organelles (nucleus or chloroplast), since they are non-coding and they replicate by RNA-RNA transcription (in a rolling cycle mode).

Viroids infect the epidermis of their hosts after mechanical damage of the plant cell wall. After entry to the first cell layers, viroids initiate replication in the nucleus or in the chloroplast and then are transported to neighbouring cells, reaching the vascular tissues and virtually all plant tissues.

The transmission of viroids is both "natural" and human-driven. Viroids are mostly transmitted via mechanical methods by contaminated machinery and tools, pruning, and other mechanic argricultural techniques. Transmission also occurs through infected seed and pollen, they don't have important natural vectors from the animal kingdom. Also contact between adjacent plants can be another (inefficient) way to transmit viriods.

I have found a reference here for further informations. It isn't open access but it is possible to watch an abundant Google preview.


21.4 Other Acellular Entities: Prions and Viroids

In this section, you will explore the following questions:

  • What are prions and how do they cause disease?
  • What are viroids and their targets of infection?

Connection for AP ® Courses

The content described in this section is outside the scope for AP ® . However, it’s interesting to note that prions and viroids—pathogens that are far simpler in structure than viruses—can produce deadly diseases, including mad cow disease and Creutzfeldt–Jakob disease. Prions are infectious proteins, whereas viroids are single-stranded RNA pathogens (agents with the ability to cause disease) that infect plants.

Prions

Prions, so-called because they are proteinaceous, are infectious particles—smaller than viruses—that contain no nucleic acids (neither DNA nor RNA). Historically, the idea of an infectious agent that did not use nucleic acids was considered impossible, but pioneering work by Nobel Prize-winning biologist Stanley Prusiner has convinced the majority of biologists that such agents do indeed exist.

Fatal neurodegenerative diseases, such as kuru in humans and bovine spongiform encephalopathy (BSE) in cattle (commonly known as “mad cow disease”) were shown to be transmitted by prions. The disease was spread by the consumption of meat, nervous tissue, or internal organs between members of the same species. Kuru, native to humans in Papua New Guinea, was spread from human to human via ritualistic cannibalism. BSE, originally detected in the United Kingdom, was spread between cattle by the practice of including cattle nervous tissue in feed for other cattle. Individuals with kuru and BSE show symptoms of loss of motor control and unusual behaviors, such as uncontrolled bursts of laughter with kuru, followed by death. Kuru was controlled by inducing the population to abandon its ritualistic cannibalism.

On the other hand, BSE was initially thought to only affect cattle. Cattle dying of the disease were shown to have developed lesions or “holes” in the brain, causing the brain tissue to resemble a sponge. Later on in the outbreak, however, it was shown that a similar encephalopathy in humans known as variant Creutzfeldt-Jakob disease (CJD) could be acquired from eating beef from animals with BSE, sparking bans by various countries on the importation of British beef and causing considerable economic damage to the British beef industry (Figure 21.18). BSE still exists in various areas, and although a rare disease, individuals that acquire CJD are difficult to treat. The disease can be spread from human to human by blood, so many countries have banned blood donation from regions associated with BSE.

The cause of spongiform encephalopathies, such as kuru and BSE, is an infectious structural variant of a normal cellular protein called PrP (prion protein). It is this variant that constitutes the prion particle. PrP exists in two forms, PrP c , the normal form of the protein, and PrP sc , the infectious form. Once introduced into the body, the PrP sc contained within the prion binds to PrP c and converts it to PrP sc . This leads to an exponential increase of the PrP sc protein, which aggregates. PrP sc is folded abnormally, and the resulting conformation (shape) is directly responsible for the lesions seen in the brains of infected cattle. Thus, although not without some detractors among scientists, the prion seems likely to be an entirely new form of infectious agent, the first one found whose transmission is not reliant upon genes made of DNA or RNA.

Viroids

Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

Viroids are known to infect plants (Figure 21.19) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.

Career Connection

Virologist

Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies (Figure 21.20) or become science writers, to name just a few possible careers.

If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.

Which of the following is not associated with prions?

Which statement is true of viroids?

Prions are responsible for variant Creutzfeldt-Jakob Disease, which has resulted in over 100 human deaths in Great Britain during the last 10 years. How do humans obtain this disease?

This prion-based disease is transmitted through human consumption of infected meat.

How are viroids like viruses?

They both replicate in a cell, and they both contain nucleic acid.

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    Cannabis Viruses, Viroids, and Phytoplasmas

    A virus is an infectious nucleic acid-based pathogen that is parasitic to the host. Essentially, it is a non-host genome that ‘hijacks’ the replication machinery of the host cell in order to amplify its genome. It also requires host enzymes to translate the viral transcripts into proteins that the virus uses to form a protective coat and move within the host/spread to alternate hosts such as insects. A virion is a viral genome encapsulated in a protein coat. Some viruses will also have a fatty membrane surrounding the protein capsid.

    There is some argument as to whether viruses can really be classified as ‘alive’. Though they have a genome, they do not have their own metabolism or replication abilities. They can really be thought of as ‘selfish genes’, meaning that they are a group of genes that evolved together in order to perpetually reproduce. They are truly an insight into the evolution of life: how replication is always selected for, seemingly without purpose in the case of a virus.

    Since they are obligate parasites, viruses generally have evolved to not kill their native host before they can reproduce enough. In the case of insect vectored viruses, this may mean interacting with the plant in such a way that the metabolism of the plant becomes more attractive to the insect vector. In the case of seed-transmitted viruses, it may mean inducing early flowering to shorten the period of time that the virus is restricted to the host, one can think of many ways that a virus can affect the phenotype of a plant to favor its spread while harming the agricultural value of the crop.

    Image from Nagy, P., & Pogany, J. (2011). The dependence of viral RNA replication on co-opted host factors. Nature Reviews. Microbiology, 10, 137–149. https://doi.org/10.1038/nrmicro2692
    and uploaded on ResearchGate

    The very first virus to ever be discovered was actually a plant virus, and one that has had some amount of interest within the Cannabis community, tobacco mosaic virus (TMV). We will discuss TMV further, but for now I will just say there is little evidence of it causing disease symptoms in Cannabis. Different plant viruses are transmitted through different means. Plant viruses are usually spread by an insect/nematode vector, through seed, through pollen, or are mechanically transmitted (usually in the setting of human agriculture).

    • Some plant viruses are limited to the plant phloem and cannot infect epidermal/mesophyll cells.. These viruses generally cause ‘yellows’ symptoms, a faily even chlorosis
    • Sap-transmissible viruses can infect epidermal/mesophyll cells and generally cause mosaic and mottling symptoms

    Generally, the phloem limited viruses are semi persistent (travel to the insect vector’s foregut) or persistent viruses (travel to the insect vector’s haemolymph and salivary glands) that are vectored exclusively by phloem-feeding insects such as aphids, whiteflies, or leafhoppers. Sap-transmissible viruses commonly cause mosaic and mottling symptoms on host tissue, whereas phloem-limited viruses tend to be ‘yellowing’ type viruses with more uniform symptoms. Many viruses are multipartite, meaning they have segmented genomes that are encapsulated separately but must all be present in the host in order to cause disease.

    Persistent viruses

    Persistent Circulative plant viruses are able to enter the haemolymph (analagous to blood) and salivary glands of their insect vectors/seconday hosts, but they do not replicate within the host cell. Peristent Propagative viruses are able to actively reproduce within the insect and also infect the insect haemolymph and salivary glands. Circulative viruses remain viable within for long periods of time (often the lifespan of the insect).

    Image from biol-2022/6524/image_S3174nee4aJmg.jpg
    Representative of circulative and propagative transmission with phloem feeding insects

    Semi-persistent viruses

    Semi-persistant viruses do not enter the haemolymph of the insect vectors, but do travel to the foregut. Some yellows and some mosaic viruses are semi-persistent. They do not take as long to acquire for the insect vector compared to circulative viruses, and the latent period is very short. They remain viable for inoculation for a few days.

    Non persistent viruses

    Nonpersistent viruses are only carried on the stylets of sucking/probing insects and remain viable for a few hours and must be quickly transmitted to a new host.

    What is a plant viroid?

    All known viroids infect plants, and most are pathogenic. Viroids are very similar to viruses except that they do not have a protein coat, they are simply self-replicating and transmissible nucleic acid pathogens. Viroids are usually spread through aphids or mechanical transmission.

    What is a plant phytoplasma?

    Phytoplasmas are very small mollicutes (bacteria that lack a cell wall). They are not much like viruses biologically, but I am including them in this particular article because the symptoms many phytoplasmas cause can be similar to those caused by viruses. In addition they are unculturable and are insect-transmissible (mostly by leafhoppers, planthoppers, and psyllids). Phytoplasmas act very similarly to circulative viruses within the insect vector, they enter the insect haemolymph and colonize the salivary glands.

    What viruses have been reported in Cannabis?

    In my opinion, viruses are significantly underdiagnosed in Cannabis and are the least understood of all pathogen classes in the species. There appears to be more research into Cannabis diseases recently, but up until the recent past, only 5 viruses were reported as commonly and naturally causing problems in commercial Cannabis production. These viruses are: Hemp streak virus (HSV), alfalfa mosaic virus (AMV), cucumber mosaic virus (CMV), arabis mosaic virus (ArMV), and hemp mosaic virus (HMV). As far as I am aware, HSV has only been reported on fiber cultivars in Europe. HMV, on the other hand, has been reported in some drug cultivars in Pakistan. AMV, CMV, and ArMV have been reported on European hemp. There is next to no information in regards to infection of modern North American drug cultivars by these viruses

    In 1971, Hartowicz et al. screened 22 common plant viruses and found that over half of them were able to infect Cannabis, but only 8 actually caused symptoms. Keep in mind that these were all manual innoculations and may not actually be vectored to Cannabis in nature. Of the manually inoculated viruses, 5 of them caused severe mosaic symptoms and plant stunting: Tobacco Ringspot Virus (TRSV), Tomato Ringspot Virus (TomRSV), Tobacco Streak Virus (TSV), and Cucumber Mosaic Virus (CMV). Two of the viruses caused mosaic symptoms but did not cause heavy stunting: Alfalfa Mosaic Virus (AMV) and Eunoymous Rinspot Virus (ERSV). Elm Mosaic Virus (EMV) also caused some symptoms of necrotic flecking.

    Most recently (2020), Beet Curly Top Virus (BCTV) was found to be a common and naturally occurring infectious agent on plants in Colorado [18]. In 2019, Lettuce Chlorosis Virus (LCV) was found in Cannabis grows in Israel [7].

    BCTV symptoms were first noticed in a field in CO in 2015. Leaves would begin yellowing in a mosaic pattern from the petiole to the tips of leaves. Plants with advanced symptoms displayed stunted growth, malformation of new leaves, leaf chlorosis, and necrotic flecking. BCTV was confirmed to be the causal agent by utilizing next generation total active RNA sequencing and using control plants to find the viral genome present. It was confirmed through PCR as well. This has been the method of discovering viruses in high value crops such as grapevine stock, and it appears to be utilized more for discovering diseases of Cannabis. BCTV is a Curtovirus within the Geminiviridae family. It is fairly unique because its genome is ssDNA instead of RNA. This means that it needs to utilize the host plant’s transcription and translation mechanisms. It has a monopartite genome that is encapsulated in a dual icosahedral capsule. It is the only virus in Cannabis that is transmitted by a leafhopper, Neoaliturus tenellus, native to the western USA. BCTV is a circulative nonpropagative virus, has a very broad host range, and can have significant impacts on yield. In some species [17], it can be transmitted by seeds, but this is unknown for Cannabis.

    BCTV In hemp. Image taken from https://durangoherald.com/articles/293876#

    HSV is reportedly one of the most common viral diseases, at least in commercial hemp in Europe. However, researchers have been unable to identify any causal agent for the symptoms associated with Hemp Streak Virus. It has long been assumed that HSV is viral and transmissible, but more recent molecular studies suggest that an abiotic factor may be at play because no pathogenic viruses were found in symptomatic Cannabis plants from screening with targeted PCR reactions and RNA sequencing [9]. It has been suggested that if this is indeed a viral disease, that it may also be responsible for certain leaf curling symptoms found on Hemp in Hungary in the late 1990s [3]. It is also reportedly vectored by aphids and seed, but this has not been demostrated experimentally. Insect vectoring would certainly point towards HSV being a vectored pathogen [3].

    HSV image: taken from biol-2022/6524/image_ENugtQ7mSeS0CQ9Wext.jpg

    I wonder if HSV symptoms may have been misdiagnosed mite damage, such as broad mites or russet mites which produce symptoms very similar to those described of HSV. Some mites may even be vectored by insects by hitching a ride The following image is taken from a plant with broad mites, and displays symptoms very similar to those described from HSV:

    The leaf in the background shows leaf curling consistent with HSV symptoms, and the leaves in the foreground show streaking symptoms.
    Image taken from https://www.growweedeasy.com/wp-content/uploads/2017/02/example-of-drooping-top-leaves-caused-by-broad-mite-damage-marijuana.jpg

    ***Please be aware that there are many online sources that believe that Sunn-Hemp Mosaic Virus is the same as HMV and claim that Sunn-Hemp Mosaic can infect Cannabis. There is absolutely no evidence of HMV being caused by SHMV, and this misidentification does not even align with reports of HMV being only an insect-vectored disease. Sunn-hemp is a legume and is a completely different plant than hemp, but the name seems to be confusing for some. Reputable websites including Dinafem’s website seem to equate Sunn-Hemp virus to Hemp Mosaic Virus without justification.***

    The causal agent of HMV is also unidentified, but has been suggested to be a Cucumovirus or a Nepovirus. It is reportedly vectored by aphids, but I have seen one report that it was vectored by onion thrips, which doesn’t make sense as no Cucumoviruses or Nepoviruses are vectored by thrips. In one experiment, an Argentine sunflower virus was inoculated onto hemp and the plant contracted HMV-like symptoms and could be transmitted by aphids [3].

    HMV causes chlorotic leaf lesions that expand, become necrotic, and can kill leaves. HMV may cause leaf enation, leaf curl, bunchy top, and reduced leaf size. Severe symptoms may look something like this:

    Image taken from: ?_nc_ht=scontent-lga3-1.cdninstagram.com&_nc_cat=109&_nc_ohc=sYxJf1-jcoYAX87iiVi&oh=5a216e8a4c195b0fb180d39831356293&oe=5EC01655

    This is simply a plant with symptoms consistent of those with HMV, it is not a confirmed diagnosis.

    Cannabis cryptic virus

    Another virus known as Cannabis cryptic virus has been identified to be ubiquitously present in Cannabis without causing any disease symptoms [8, 9]. Virions were visualized and sequences were obtained, but viral presence does not seem to be correlated to symptoms. The cryptic virus appears to be a Partitivirus which is likely seed transmissible [16].

    Lettuce Chlorosis Virus

    Recently (2019), a new virus was reported in Cannabis. LCV is a Crinivirus within the Closteroviridae. Lettuce Chlorosis Virus (LCV) was reported as causing interveinal chlorosis, leaf brittleness, and necrotic spots in licensed Cannabis grows in Israel. The virus was shown to be transmissible by the whilefly species Bemisia tabici [7]. LCV was not found to be seed transmissible, but can be transmitted by vegetative propagation.

    AMV is an Alfamovirus within the Bromoviridae. AMV was first identified on hemp in Germany through sap transmission tests. It is most commonly spread through aphid and seed/clone transmission, but can also be spread through dodder or root grafts. It is a ssRNA virus and the genome is split between 4 virions.

    Symptoms include leaf chlorosis in a mosaic or mottle pattern, sometimes presenting as a gray mosaic. Young leaves may have strange morphology (puckering).

    Image taken from https://www.google.com/url?sa=i&url=https%3A%2F%2Fallcropsolutions.com%2Fdisease-testing%2Fhemp-and-hop-diseases%2F&psig=AOvVaw2ErtK3TxRV9yr9hAMiwN2l&ust=1584083662267000&source=images&cd=vfe&ved=0CAIQjRxqFwoTCLDUjtqxlOgCFQAAAAAdAAAAABAD
    It is claimed to be AMV on Cannabis, though the diagnosis cannot be confirmed

    An example of AMV on tobacco is shown below, demonstrating the leaf puckering and chlorotic mosaic:

    Image taken from biol-2022/6524/image_OuPq5kVxtSfIAgn389r.jpg?itok=sP6CFHK3

    The following Cannabis leaf shows some very minor puckering as well as mosaic symptoms:

    Image taken from: https://www.rollitup.org/proxy.php?image=https%3A%2F%2Fwww.thcfarmer.com%2Fcommunity%2Fattachments%2Fdsc03378-jpg.275131%2F&hash=64fe3a9a4288140b02e7d5d3efdae5b2

    ArMV is a Nepovirus within the Secoviridae family. Both CMV and ArMV are tripartite viruses that cause similar symptoms. ArMV has been described as causing chlorotic spots and stripes, and has also been described as displaying symptoms of chlorotic ‘check mark’ shapes [3]. It appears to have a negative impact on the growth of the plant as well. ArMV has a broad host range. It infects many vegetables, and also infects hops. It is primarily transmitted by nematodes, but may also be seed transmissible in many species and can be transmitted by vegetative propagation (cloning).

    CMV is a tripartite Cucumovirus. It is within the Bromoviridae like AMV. It has a very broad host range and has been found on dicots and monocots including various vegetable, ornamental, and grass crops [15]. It is vectored by aphids and is also seed transmissible in many species. It will also be transmitted by cloning. This will be difficult to distinguish from other mosaic viruses, but has been described as having light green ‘check mark’ chlorosis, similar to that described for ArMV [3]. An image of such symptoms on Cannabis is shown below, but I am not sure which virus is causing this:

    Can TMV Infect Cannabis?

    In Hartowicz et al., they also mention that TMV is indeed able to infect Cannabis, but it did not cause any noticeable symptoms [2, 3] rather, Cannabis appears to act as a carrier for the virus. They confirmed the presence of TMV in nonsymptomatic Cannabis by back-inoculating to indicator plants. It seems that in almost every Cannabis forum site or popular media site, it is commonly reported that TMV can cause symptoms in Cannabis. However, these claims are usually uncited and unsubstantiated. In fact, in the cases of people actually posting serological test results of plants with mosaic symptoms, I have never seen a positive result for TMV. Of course, different cultivars of Cannabis may react differently to infection by TMV and some may actually produce noticeable symptoms that were not seen in experiments conducted on hemp cultivars. While it may be possible for TMV to cause symptoms in Cannabis, based on published information, it is more likely that TMV is symptomless in Cannabis and that mosaic symptoms are caused by viruses that have been reported to affect the health of Cannabis plants.

    A farmer once reported that he infected a Cannabis plant with a tobacco virus that caused stunting and mosaic symptoms, but it is speculated that virus transferred was Tomato ringspot virus, Tobacco rinspot virus, or Tobacco streak virus as these can all infect Cannabis in cases of mechanical inoculation and are sap transmissible [3].

    What Insects Vector Viruses in Cannabis?

    According to Ceapoiu (1958), the worst vectors of Cannabis viruses are bhang aphids (Phorodon cannabis), greenhouse whiteflies (Trialeudodes vaporariorum), onion thrips (Thrips tabaci) and green peach aphids (Myzus persicae). P. cannabis has been shown to vector at least 2 viruses to Cannabis: CMV and AMV [5]. P. cannabis has also been shown to vector Pea Mosaic Virus in the lab [6], but I am unaware of any cases of natural infection of PMV in Cannabis. In 1955, P. cannabis was also reported to be the vector for HSV [3], though as mentioned earlier, it is still unknown if HSV is actually a viral disease. P. cannabis has also been reported to vector Hemp Mosaic Virus (HMV), though molecular evidence of this is lacking [4]. Much like HSV, the causal agent of HMV has not been identified and confirmation of insect vectoring has not occurred [7].

    Despite T. vaporariorum being reported as a vector for Cannabis viruses, there is no information in the literature as to which Cannabis diseases it may vector. The only viruses shown to be vectored by T. vaporariorum in plants are within the Crinivirus genus. The only confirmed crinivirus in Cannabis is the recently reported Lettuce Chlorosis Virus, which was reported B. tabaci as a likely vector, but T. vaporariorum may be able to vector this virus as well.

    In regards to thrips, the two main species affecting Cannabis are onion thrips (Thrips tabaci) and western flower thrips (Frankliniella
    occidentalis
    ) [10]. Again, there is no evidence here of whether or not any viruses are actually vectored by thrips in Cannabis. The only viruses known to be vectored by thrips are within the Tospovirus genus, none of which have been reported in Cannabis. Of course, this does not mean that tospoviruses don’t affect Cannabis or that thrips do not transmit viruses, just that there is not yet evidence of this.

    Green peach aphids (Myzus persicae) have also been reported as vectors in Cannabis. They are at least capable of transmitting AMV, CMV [11, 12], but it is unknown what other viruses they may vector.

    In regards to ArMV, it appears that it is most readily vectored by dagger nematodes within the genus Xiphinema [13]. However, no Xiphenema species have every been reported on Cannabis. Despite an uncited claim on Wikipedia, ArMV has not been demonstrated to be vectored by insects such as aphids or whiteflies, but may be able to be transmitted by other genera of nematodes such as needle nematodes withing the Longidorus genus [14].

    BCTV is the only Cannabis virus to be vectored by a leafhopper (specifically Neoaliturus tenellus, at least that is the only reported vector of BCTV on the wide range of hosts it can infect.

    What to do if you suspect your plant(s) have a virus

    First off, there is no easy answer to this. There is no ‘cure’ to viral diseases there is no spray that will eliminate the problem for you. Growers have to be on top of insect control, proper sanitation, and culling of infected plants in order to prevent infection in the first place. Of course, sourcing virus-free growing stock (seeds or clones) is of upmost importance.

    Second, it is important to have an IPM program in place to control insects that may be vectors for viruses. I would say that aphids and whiteflies are the two biggest threats as insect vectors.

    For all pathogens covered in this article including viruses, viroids, and phytoplasmas, one of the simplest things you can do to prevent spread is to practice sanitation such as sterilizing your tools with 70% alcohol between each cut or plant, to sterilize your indoor facility after each grow, and to practice cleanliness in your grow areas and what you wear in your grow areas. It is never a bad idea to shower before going into your grow area, wear scrubs that you wash frequently, and have dedicated boots that your sterilize the soles of frequently.

    What Viroids Infect Cannabis?

    As of now, the only viroid that has been reported in Cannabis is the Hop Latent Viroid (HpLVd) [19]. It is a 256 bp circular RNA within the Cocadviroid family. It was identified by Dr. Jeremy Warren at Dark Heart Nursery through total RNA sequencing of symptomatic plants. It was confirmed as the disease-causing agent through development of infectious RNA constructs and RT-PCR of infected plants. In Cannabis, the disease is known Cannabis Dudding. Plants with Dudding may have reduced vigor, smaller size, more stretch and weaker branching, and small leaves in vegetative growth:

    Image taken from biol-2022/6524/image_9uyy5zkkDMsEdlx5w0.jpg

    In flower, buds lack trichome development, terpenes are reduced, bud is more leafy and more airy (larfy), buds can be irregularly shaped, chlorosis and leaf death may occur, and buds appear behind schedule. In the following picture, the cola on the left is from a healthy plant, and the cola on the right is from a dudded plant.:

    The infected bud does look frosty in this picture, but the lack of density and high amount of vegetative growth is evident. The following picture shows dried buds from the same plants:

    Image taken from .556818/

    Dark Heart nursery has been able to provide clean stock by doing tissue culture to produce mother plants. This is a process where cells from the very tip of the apical meristem are cultured and generated into a new plant, and many viruses and viroids have not yet been able to infect the newest growth of plants. HpLVd does not appear to be insect-vectored, but is transmitted through mechanical means, usually by using non-sterile shears and tools on plants. It may be transmissible by seed at low rates as well.

    To prevent HpLVd, it is important to begin with clean stock and use proper cultural controls in your grow including spraying tools with 70% ethanol in between each plant.

    What Phytoplasmas Infect Cannabis?

    Cannabis is susceptible to a wide range of phytoplasmas.

    • In 2007, hemp witches’ broom in China was identified as a phytoplasma in the Elms Yellows (EY) group [21].
    • In 2011, hemp witches’ broom in Iran was confirmed to be caused by a phytoplasma in the stolbur group. [20].
    • In 2015, Cannabis sativa was identified as a host for the asteris group of phytoplasma in India [22].
    • In 2019, C. sativa was identified as a host for the trifolii group of phytoplasma in NV, U.S.A. [23].

    All of these phytoplasmas were identified through nested PCR using conserved phytoplasma primers followed by sequencing.

    Phytoplasma symptoms in Cannabis can include:

    • A high amount of branch proliferation from a branch node
    • Shortened internode spacing
    • Small leaves or leaf dieback
    • Phyllody (abnormal development of flowers as leafy structures.

    What vectors phytoplasmas in Cannabis?

    The primary vectors of phytoplasmas are leafhoppers, planthoppers, and psyllids [25].In India, the leafhopper Hishimonas phycitis was found to vector the asteris phytoplasma and is the putative vector in Cannabis [24]. Elms yellows diseases are usually transmitted via leafhoppers. Stolbur group phytoplasmas are frequently transmitted by planthopper species. Trifolii group phytoplasmas are frequently transmitted by leafhopper species.

    Image from biol-2022/6524/image_Tkxds7bu9L6lnmJzDo3.png

    Phytoplasma Control

    Generally, Phytoplasma diseases are controlled by preventing infection through insect control. Some phytoplasmas can be seed transmissible, but this has not been demonstrated in Cannabis. Phytoplasma diseases may be able to be controlled through application of antibiotics such as tetracycline and rifampicin [26], but these are not approved for commercial production anywhere that I am aware of. A plant genotype can be recovered through meristematic tissue culture, but once infected, a plant will not produce well or have marketable bud.

    In short, viruses, phytoplasmas, and viroids are mostly controlled through prevention and include virus free seed, tissue cultured clones, and insect control. One a plant has one of these problems, it will not be able to be treated and will not be worth producing with. In fact, it is important to cull any plants you find with these symptoms unless you want to preserve the plant’s genetics, in which it may be worth having the plant go through tissue culture.

    I hope this article shed light on the confusion surrounding these types of diseases in Cannabis and addressed some of the misinformation commonly spread on forums and message boards.


    108 Other Acellular Entities: Prions and Viroids

    By the end of this section, you will be able to do the following:

    • Describe prions and their basic properties
    • Define viroids and their targets of infection

    Prions and viroids are pathogens (agents with the ability to cause disease) that have simpler structures than viruses but, in the case of prions, still can produce deadly diseases.

    Prions

    Prions , so-called because they are proteinaceous, are infectious particles—smaller than viruses—that contain no nucleic acids (neither DNA nor RNA). Historically, the idea of an infectious agent that did not use nucleic acids was considered impossible, but pioneering work by Nobel Prize-winning biologist Stanley Prusiner has convinced the majority of biologists that such agents do indeed exist.

    Fatal neurodegenerative diseases, such as kuru in humans and bovine spongiform encephalopathy (BSE) in cattle (commonly known as “mad cow disease”) were shown to be transmitted by prions. The disease was spread by the consumption of meat, nervous tissue, or internal organs between members of the same species. Kuru, native to humans in Papua New Guinea, was spread from human to human via ritualistic cannibalism. BSE, originally detected in the United Kingdom, was spread between cattle by the practice of including cattle nervous tissue in feed for other cattle. Individuals with kuru and BSE show symptoms of loss of motor control and unusual behaviors, such as uncontrolled bursts of laughter with kuru, followed by death. Kuru was controlled by inducing the population to abandon its ritualistic cannibalism.

    On the other hand, BSE was initially thought to only affect cattle. Cattle dying of the disease were shown to have developed lesions or “holes” in the brain, causing the brain tissue to resemble a sponge. Later on in the outbreak, however, it was shown that a similar encephalopathy in humans, known as variant Creutzfeldt-Jakob disease (CJD), could be acquired from eating beef from animals infected with BSE, sparking bans by various countries on the importation of British beef and causing considerable economic damage to the British beef industry ((Figure)). BSE still exists in various areas, and although a rare disease, individuals that acquire CJD are difficult to treat. The disease can be spread from human to human by blood, so many countries have banned blood donation from regions associated with BSE.

    The cause of spongiform encephalopathies, such as kuru and BSE, is an infectious structural variant of a normal cellular protein called PrP (prion protein). It is this variant that constitutes the prion particle. PrP exists in two forms, PrP c , the normal form of the protein, and PrP sc , the infectious form. Once introduced into the body, the PrP sc contained within the prion binds to PrP c and converts it to PrP sc . This leads to an exponential increase of the PrP sc protein, which aggregates. PrP sc is folded abnormally, and the resulting conformation (shape) is directly responsible for the lesions seen in the brains of infected cattle. Thus, although not without some detractors among scientists, the prion seems likely to be an entirely new form of infectious agent, the first one found whose transmission is not reliant upon genes made of DNA or RNA.


    Viroids

    Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

    Viroids are known to infect plants ((Figure)) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.


    Virologist
    Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies ((Figure)) or become science writers, to name just a few possible careers.


    If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.

    Section Summary

    Prions are infectious agents that consist of protein, but no DNA or RNA, and seem to produce their deadly effects by duplicating their shapes and accumulating in tissues. They are thought to contribute to several progressive brain disorders, including mad cow disease and Creutzfeldt-Jakob disease. Viroids are single-stranded RNA pathogens that infect plants. Their presence can have a severe impact on the agriculture industry.

    Review Questions

    Which of the following is not associated with prions?

    Which statement is true of viroids?

    1. They are single-stranded RNA particles.
    2. They reproduce only outside of the cell.
    3. They produce proteins.
    4. They affect both plants and animals.

    Critical Thinking Questions

    Prions are responsible for variant Creutzfeldt-Jakob Disease, which has resulted in over 100 human deaths in Great Britain during the last 10 years. How do humans contract this disease?

    This prion-based disease is transmitted through human consumption of infected meat.

    How are viroids like viruses?

    They both replicate in a cell, and they both contain nucleic acid.

    A botanist notices that a tomato plant looks diseased. How could the botanist confirm that the agent causing disease is a viroid, and not a virus?

    The botanist would need to isolate any foreign nucleic acids from infected plant cells, and confirm that an RNA molecule is the etiological agent of disease. The botanist would then need to demonstrate that the RNA can infect plant cells without a capsid, and that the RNA replicates, but is not translated to produce proteins.

    Glossary


    Viroids

    Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

    Viroids are known to infect plants ([link]) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.


    Virologist
    Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies ([link]) or become science writers, to name just a few possible careers.


    If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.


    How are viruses, viroids and prions related?

    We're all familiar with the basics of viruses: These particles infect living cells and basically wreak havoc throughout the body. But viruses aren't the only villains around causing chaos in living things. Other infectious agents called viroids and prions — which are also tiny but powerful — can take down both plant life and entire animals.

    How are viroids and prions the same as viruses? And how are they different? All three — viruses, viroids, and prions — are acellular particles. Acellular particles are not alive, which means:

    • They're not made of cells.
    • They don't transform energy.
    • They can't reproduce on their own.
    • They can only be seen with an electron microscope.
    • They don't grow or divide.

    Acellular particles can hang around forever — sitting on a countertop or on a doorknob, doing nothing and causing no harm. However, viruses, viroids and prions are infectious agents. Once they enter a suitable cell, be it animal, plant or bacterial, they take over the cell's metabolic agents to increase their own numbers [source: Paustian].

    You can almost think of them as hijackers. The only goal for viruses, viroids and prions is reproduction, and the only way for them to achieve that goal is to take over host cells. Once they take over, they use those cells to alter normal functioning and make new virus particles. These particles can cause disease in plants, animals and humans — and they've even changed the history of life on Earth by changing the DNA of various organisms.

    Now let's look at how the three are different, starting with viruses.

    A virus is a package of genetic material. This genetic material is either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA). This little package is carried in a shell called the capsid. Some viruses have an extra envelope covering the capsid. While covered in its capsid, a virus is in an extracellular state. This means the virus hasn't invaded a host cell and is pretty much just hanging around doing nothing.

    However, once a virus invades a host cell, it becomes intracellular, and that's when the action starts. A virus can infect a cell several different ways — through bodily fluids (such as saliva or blood), air (sneezing or coughing) or a mosquito bite. The virus then begins its attack by triggering the cell to let it in and take control. The virus starts replicating and overriding the cell's normal functioning and, in some cases, inserts its own genetic material into the cell's DNA. The cell actually does all the work — the virus just calls the shots. The virus becomes a commander and starts sending out more infectious troops into the body.

    Even though the body has natural defenses against viruses, many viral infections replicate so rapidly that our immune system simply can't keep up. Antibiotics are useless against viruses, although immunizations work. Common examples of viruses include:


    21.4 Other Acellular Entities: Prions and Viroids

    By the end of this section, you will be able to do the following:

    • Describe prions and their basic properties
    • Define viroids and their targets of infection

    Prions and viroids are pathogens (agents with the ability to cause disease) that have simpler structures than viruses but, in the case of prions, still can produce deadly diseases.

    Prions

    Prions , so-called because they are proteinaceous, are infectious particles—smaller than viruses—that contain no nucleic acids (neither DNA nor RNA). Historically, the idea of an infectious agent that did not use nucleic acids was considered impossible, but pioneering work by Nobel Prize-winning biologist Stanley Prusiner has convinced the majority of biologists that such agents do indeed exist.

    Fatal neurodegenerative diseases, such as kuru in humans and bovine spongiform encephalopathy (BSE) in cattle (commonly known as “mad cow disease”) were shown to be transmitted by prions. The disease was spread by the consumption of meat, nervous tissue, or internal organs between members of the same species. Kuru, native to humans in Papua New Guinea, was spread from human to human via ritualistic cannibalism. BSE, originally detected in the United Kingdom, was spread between cattle by the practice of including cattle nervous tissue in feed for other cattle. Individuals with kuru and BSE show symptoms of loss of motor control and unusual behaviors, such as uncontrolled bursts of laughter with kuru, followed by death. Kuru was controlled by inducing the population to abandon its ritualistic cannibalism.

    On the other hand, BSE was initially thought to only affect cattle. Cattle dying of the disease were shown to have developed lesions or “holes” in the brain, causing the brain tissue to resemble a sponge. Later on in the outbreak, however, it was shown that a similar encephalopathy in humans, known as variant Creutzfeldt-Jakob disease (CJD), could be acquired from eating beef from animals infected with BSE, sparking bans by various countries on the importation of British beef and causing considerable economic damage to the British beef industry (Figure 21.17). BSE still exists in various areas, and although a rare disease, individuals that acquire CJD are difficult to treat. The disease can be spread from human to human by blood, so many countries have banned blood donation from regions associated with BSE.

    The cause of spongiform encephalopathies, such as kuru and BSE, is an infectious structural variant of a normal cellular protein called PrP (prion protein). It is this variant that constitutes the prion particle. PrP exists in two forms, PrP c , the normal form of the protein, and PrP sc , the infectious form. Once introduced into the body, the PrP sc contained within the prion binds to PrP c and converts it to PrP sc . This leads to an exponential increase of the PrP sc protein, which aggregates. PrP sc is folded abnormally, and the resulting conformation (shape) is directly responsible for the lesions seen in the brains of infected cattle. Thus, although not without some detractors among scientists, the prion seems likely to be an entirely new form of infectious agent, the first one found whose transmission is not reliant upon genes made of DNA or RNA.

    Viroids

    Viroids are plant pathogens: small, single-stranded, circular RNA particles that are much simpler than a virus. They do not have a capsid or outer envelope, but like viruses can reproduce only within a host cell. Viroids do not, however, manufacture any proteins, and they only produce a single, specific RNA molecule. Human diseases caused by viroids have yet to be identified.

    Viroids are known to infect plants (Figure 21.18) and are responsible for crop failures and the loss of millions of dollars in agricultural revenue each year. Some of the plants they infect include potatoes, cucumbers, tomatoes, chrysanthemums, avocados, and coconut palms.

    Career Connection

    Virologist

    Virology is the study of viruses, and a virologist is an individual trained in this discipline. Training in virology can lead to many different career paths. Virologists are actively involved in academic research and teaching in colleges and medical schools. Some virologists treat patients or are involved in the generation and production of vaccines. They might participate in epidemiologic studies (Figure 21.19) or become science writers, to name just a few possible careers.

    If you think you may be interested in a career in virology, find a mentor in the field. Many large medical centers have departments of virology, and smaller hospitals usually have virology labs within their microbiology departments. Volunteer in a virology lab for a semester or work in one over the summer. Discussing the profession and getting a first-hand look at the work will help you decide whether a career in virology is right for you. The American Society of Virology’s website is a good resource for information regarding training and careers in virology.

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      Special Issue Editor

      Viroid is the smallest pathogen consisting of a circular single-stranded RNA of

      250&ndash400 nucleotides. Despite its nature of non-coding RNA, once it has entered a host cell, viroid replicates relying on the host transcription machinery and spreads from the infected cells throughout the plant, causing virtually asymptomatic to very severe disease symptoms.

      Such biological functions of viroids are generated by direct and indirect interactions between molecular elements embedded in the highly structured viroid RNA or viroid-derived small RNAs produced by RNA silencing targeting the viroid and host factors involved in the regulation of defense or development. In fact, even a point mutation can alter the pathogenicity, host specificity, or transmission of viroids however, understanding the underlying mechanisms awaits further analysis.

      In this Special Issue, we will focus on the latest information on the molecular functions of viroids and on viroid diseases and call for submission of manuscripts on the molecular factors in viroid RNA that control replication, transport, transmission or pathogenicity, on the impact of viroid infection on the host transcriptome or metabolome, and on host genes, microRNAs, transcription factors, etc. that are involved in the development of specific viroid diseases.

      Dr. Teruo Sano
      Guest Editor

      Manuscript Submission Information

      Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

      Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

      Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


      RNA viruses

      Class III: dsRNA

      Double-stranded RNA viruses infect bacteria, fungi, plants, and animals, such as the rotavirus that causes diarrheal illness in humans. But cells do not utilize dsRNA in any of their processes and have systems in place to destroy any dsRNA found in the cell. Thus the viral genome, in its dsRNA form, must be hidden or protected from the cell enzymes. Cells also lack RNA-dependent RNA-polymerases, necessary for replication of the viral genome so the virus must provide this enzyme itself. The viral RNA-dependent RNA polymerase acts as both a transcriptase to transcribe mRNA, as well as a replicase to replicate the RNA genome.

      For the rotavirus, the viral nucleocapsid remains intact in the cytoplasm with replication events occurring inside, allowing the dsRNA to remain protected. Messenger RNA is transcribed from the minus-strand of the RNA genome and then translated by the host ribosome in the cytoplasm. Viral proteins aggregate to form new nucleocapsids around RNA replicase and plus-strand RNA. The minus-strand RNA is then synthesized by the RNA replicase within the nucleocapsid, once again insuring protection of the dsRNA genome.

      Class IV: +ssRNA

      Viruses with plus-strand RNA, such as poliovirus, can use their genome directly as mRNA with translation by the host ribosome occurring as soon as the unsegmented viral genome gains entry into the cell. One of the viral genes expressed yields an RNA-dependent RNA-polymerase (or RNA replicase), which creates minus-strand RNA from the plus-strand genome. The minus-strand RNA can be used as a template for more plus-strand RNA, which can be used as mRNA or as genomes for the newly forming viruses.

      +ssRNA.

      Translation of the poliovirus genome yields a polyprotein, a large protein with protease activity that cleaves itself into three smaller proteins. Additional cleavage activity eventually yields all the proteins needed for capsid formation, as well as an RNA-dependent RNA-polymerase.

      The formation of a polyprotein that is cut into several smaller proteins illustrates one possible strategy to an issue faced by many +ssRNA viruses &ndash how to generate multiple proteins from an unsegmented +ssRNA genome? Other possibilities include:

      • subgenomic mRNA &ndash during translation, portions of the viral RNA may be skipped, resulting in different proteins than what is made from the viral RNA in its entirety.
      • ribosomal frame-shifting &ndash the ribosome &ldquoreads&rdquo the mRNA in groups of three nucleotides or codon, which translate to one amino acid. If the ribosome starts with nucleotide #1, that is one open reading frame (ORF), resulting in one set of amino acids. If the ribosome were to move forward where nucleotide 2 is the starting nucleotide that would be ORF #2, resulting in a completely different set of amino acids. If the ribosome were to move forward again where nucleotide 3 is the starting nucleotide that would be ORF#3, resulting in an entirely different set of amino acids. Some viruses have viral genes that deliberately overlap within different ORFs, leading to the production of different proteins from a single mRNA.
      • readthrough mechanism &ndash a viral genome can have stop codons embedded throughout the sequence. When the ribosome comes to a stop codon it can either stop, ending the amino acid sequence, or it can ignore the stop codon, continuing on to make a longer string of amino acids. For viruses with the readthrough mechanism, they acquire a variety of proteins by having stop codons that are periodically ignored. Sometimes this function is combined with the ribosomal frame-shifting to produce an even greater variety of viral proteins.

      Class V: -ssRNA

      Minus-strand RNA viruses include many members notable for humans, such as influenza virus, rabies virus, and Ebola virus. Since the genome of minus-strand RNA viruses cannot be used directly as mRNA, the virus must carry an RNA-dependent RNA-polymerase within its capsid. Upon entrance into the host cell, the plus-strand RNAs generated by the polymerase are used as mRNA for protein production. When viral genomes are needed the plus-strand RNAs are used as templates to make minus-strand RNA.

      Class VI: +ssRNA, retroviruses

      Despite the fact that the retroviral genome is composed of +ssRNA, it is not used as mRNA. Instead, the virus uses its reverse transcriptase to synthesize a piece of ssDNA complementary to the viral genome. The reverse transcriptase also possesses ribonuclease activity, which is used to degrade the RNA strand of the RNA-DNA hybrid. Lastly, the reverse transcriptase is used as a DNA polymerase to make a complementary copy to the ssDNA, yielding a dsDNA molecule. This allows the virus to insert its genome, in a dsDNA form, into the host chromosome, forming a provirus. Unlike a prophage, a provirus can remain latent indefinitely or cause the expression of viral genes, leading to the production of new viruses. Excision of the provirus does not occur for gene expression.


      Difference Viruses Viroids Prions

      Infectious disease can result of cellular organisms, such as bacteria (prokaryotes), from eukaryotes (cells like ours) or from nonliving infectious agents such as viruses, virioids and prions. Here is a summery of the different types of acellular, nonliving infectious agents.

      Living things are constructed of cells and can be unicellular (one cell) or multicellular (many cells).

      Limits on Cell Size: Cells size is limited because cells must be able to exchange materials with their surroundings, and surface area relative to the volume decreases as size of cell increases. This limits the size of cells.

      Cell Theory: The basic rules that apply to these smallest units of life state:

      * All organisms are composed of one or more cells.
      * Cells are the basic unit of structure and function in organisms.
      * All cells come only from other cells.

      * Acellular Particles: Viruses, Viroids & Prions *

      Although they may seem to behave like living things, acellular particles are not alive.

      * are not made of cells
      * cannot reproduce on their own
      * do not grow or undergo division
      * do not transform energy
      * lack machinery for protein synthesis
      * are so small that they can only be seen with an electron microscope

      Viruses infect living cells and once inside, transform the cell essentially into a factory for making more viruses. These acellular particles are composed of nucleic acid (genetic material), proteins and, in some cases, lipids as well.

      Viruses reproduce via four basic steps. Viral reproduction includes:

      1. Delivery of the viral genetic material into a host cell
      2. Commandeering of the host cell transcription and translation machinery
      3. Use of the host cell’s building blocks to copy viral genomes and synthesize viral proteins
      4. Viral genomes and proteins then self-assemble and exit host cells as new infectious particles.

      Viruses exist in one of two states extracellular and intracellular.

      Extracellular State: Before it invades a host cell, a virus is in the ‘extracellular state’. An extracellular virus, called a virion (vie-ree-on), consists of a protein coat (capsid) surrounding nucleic acid. In addition, some viruses have phospholipid envelope surrounding the capsid.

      Intracellular State: Once the virus invades a host cell it is in an ‘intracellular state.’ In this state, the capsid is removed and the virus exists as only as nucleic acid (genetic material).

      Viroids are smallest known agents of infectious disease. Whereas viruses are made up of nucleic acid encapsulated in protein (capsid), viroids are uniquely characterized by the absence of a capsid. Thus far, this type of acellular particle has only been identified as an infectious agent in plants.

      Prions are an abnormal form of a normally harmless protein that cause various fatal neurodegenerative diseases called Transmissible Spongiform Encephalopathies. Once present in the brain, prions cause normal proteins to refold into abnormal shapes, destroying neurons and eventually causing the brain to become riddled with holes.

      Bauman, R. (2005) Microbiology.
      Park Talaro, K. (2008) Foundations in Microbiology.


      Watch the video: VIROIDS (September 2022).


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