Mycovirus
Mycoviruses (
True mycoviruses demonstrate an ability to be transmitted to infect other healthy fungi. Many double-stranded RNA elements that have been described in fungi do not fit this description, and in these cases they are referred to as
History
The first record of an economic impact of mycoviruses on fungi was recorded in cultivated mushrooms (Agaricus bisporus) in the late 1940s and was called the La France disease.[5] Hollings found more than three different types of viruses in the abnormal sporophores. This report essentially marks the beginning of mycovirology.[4]
The La France Disease is also known as X disease, watery stripe, dieback and brown disease.
- Reduced yield
- Slow and aberrant mycelialgrowth
- Waterlogging of tissue
- Malformation
- Premature maturation
- Increased post-harvest deterioration (reduced shelf life)[6]
Mushrooms have shown no resistance to the virus, and so control has been limited to
Perhaps the best known mycovirus is
Taxonomy
The majority of mycoviruses have double-stranded RNA (dsRNA) genomes and isometric particles, but approximately 30% have positive-sense, single-stranded RNA (+ssRNA) genomes.[1][2] However, negative single-stranded RNA viruses and single-stranded DNA viruses have also been described.[9][10][11] The updated 9th ICTV report on virus taxonomy[12] lists over 90 mycovirus species covering 10 viral families, of which 20% were not assigned to a genus or, in some cases, not even to a family.
Isometric forms predominate mycoviral morphologies in comparison to rigid rods,
Host range and incidence
Mycoviruses are common in fungi (Herrero et al., 2009) and are found in all four phyla of the true fungi: Chytridiomycota, Zygomycota, Ascomycota and Basidiomycota. Fungi are frequently infected with two or more unrelated viruses and also with defective dsRNA and/or satellite dsRNA.[14][15] There are also viruses that simply use fungi as vectors and are distinct from mycoviruses because they cannot reproduce in the fungal cytoplasm.[16]
It is generally assumed that the natural host range of mycoviruses is confined to closely related vegetability compatibility groups or VCGs which allow for cytoplasmic fusion,
In one study, forty patients with acute lymphoblastic leukemia were found to have antibodies to a mycovirus-containing Aspergillus flavus.In another research report, exposure of mononuclear cells from patients with acute lymphoblastic leukemia in full remission resulted in the re-development of the genetic and cell surface phenotypes characteristic of acute lymphoblastic leukemia
Origin and evolution
Viruses consisting of dsRNA as well as ssRNA are assumed to be very ancient and presumably originated from the "
It has also been suggested that it is very likely that plant viruses containing a movement protein evolved from mycoviruses by introducing an extracellular phase into their life cycle rather than eliminating it. Furthermore, the recent discovery of an ssDNA mycovirus has tempted some researchers[10] to suggest that RNA and DNA viruses might have common evolutionary mechanisms. However, there are many cases where mycoviruses are grouped together with plant viruses. For example, CHV1 showed phylogenetic relatedness to the ssRNA genus Potyvirus,[25] and some ssRNA viruses, which were assumed to confer hypovirulence or debilitation, were often found to be more closely related to plant viruses than to other mycoviruses.[1] Therefore, another theory arose that these viruses moved from a plant host to a plant pathogenic fungal host or vice versa. This "plant virus hypothesis" may not explain how mycoviruses developed originally, but it could help to understand how they evolved further.[citation needed]
Transmission
A significant difference between the genomes of mycoviruses to other viruses is the absence of genes for ‘cell-to-cell movement’ proteins. It is therefore assumed that mycoviruses only move intercellularly during cell division (e.g. sporogenesis) or via hyphal fusion.[14][26] Mycoviruses might simply not need an external route of infection as they have many means of transmission and spread due to their fungal host’s life style:
- Plasmogamy and cytoplasmic exchange over extended periods of time
- Production of vast amounts of asexual spores
- Overwintering via sclerotia[27]
- More or less effective transmission into sexual spores
However, there are potential barriers to mycovirus spread due to vegetative incompatibility and variable transmission to sexual spores. Transmission to sexually produced spores can range from 0% to 100% depending on the virus-host combination.[14] Transmission between species of the same genus sharing the same habitat has also been reported including Cryphonectria (C. parasitica and C. sp), Sclerotinia (Sclerotinia sclerotiorum and S. minor), and Ophiostoma (O. ulmi and O. novo-ulmi).[28][29] Intraspecies transmission has also been reported[30] between Fusarium poae and black Aspergillus isolates. However, it is not known how fungi overcome the genetic barrier; whether there is some form of recognition process during physical contact or some other means of exchange, such as vectors. Research[31] using Aspergillus species indicated that transmission efficiencies might depend on the hosts viral infection status (infected with no, different, or same virus), and that mycoviruses might play a role in the regulation of secondary mycoviral infection. Whether this is also true for other fungi is not yet known. In contrast to acquiring mycoviruses spontaneously, the loss of mycoviruses seems very infrequent[31] and suggests that either viruses actively moved into spores and new hyphal tips, or the fungus might facilitate the mycoviral transport in some other way.
Movement of mycoviruses within fungi
Although it is not known yet whether viral transport is an active or passive process, it is generally assumed that fungal viruses move forward by plasma streaming.
Impact on host phenotype
Phenotypic effects of mycoviral infections can vary from advantageous to deleterious, but most of them are asymptomatic or cryptic. The connection between phenotype and mycovirus presence is not always straight forward. Several reasons may account for this. First, the lack of appropriate infectivity assays often hindered the researcher from reaching a coherent conclusion.[35] Secondly, mixed infection or unknown numbers of infecting viruses make it very difficult to associate a particular phenotypic change with the investigated virus.[citation needed]
Although most mycoviruses often do not seem to disturb their host’s fitness, this does not necessarily mean they are living unrecognized by their hosts. A neutral co-existence might just be the result of a long co-evolutionary process.[36][37] Accordingly, symptoms may only appear when certain conditions of the virus-fungus-system change and get out of balance. This could be external (environmental) as well as internal (cytoplasmic). It is not known yet why some mycoviruses-fungus-combinations are typically detrimental while others are asymptomatic or even beneficial. Nevertheless, harmful effects of mycoviruses are economically interesting, especially if the fungal host is a phytopathogen and the mycovirus could be exploited as biocontrol agent. The best example is represented by the case of CHV1 and C. parasitica.[14] Other examples of deleterious effects of mycoviruses are the ‘La France’ disease of A. bisporus[5][38] and the mushroom diseases caused by Oyster mushroom spherical virus[39] and Oyster mushroom isometric virus.[38]
In summary, the main negative effects of mycoviruses are:
- Decreased growth rate[40]
- Lack of sporulation[40]
- Change of virulence[41][42][21]
- Reduced germination of spores[43]
Hypovirulent phenotypes do not appear to correlate with specific genome features and it seems there is not one particular metabolic pathway causing hypovirulence but several.
Classification
Most fungal viruses belong to double-stranded RNA viruses, but about 30% belong to positive-strand RNA virus.[1] However, negative single-stranded RNA viruses and single-stranded DNA viruses have also been described.[9][11][48][10] The ninth edition of the report of the International Committee on Taxonomy of Viruses lists more than 90 fungal viruses belonging to 10 families, of which about 20% of the viruses have not been incertae sedis due to insufficient sequence data and have not yet been determined.[12] The shape of most fungal viruses is isometric.[13]
References
49.Tebbi CK, Badiga A, Sahakian E, Arora AI, Nair S, Powers JJ, Achille AN, Jaglal MV, Patel S, Migone F. Plasma of Acute Lymphoblastic Leukemia Patients React to the Culture of a Mycovirus Containing Aspergillus flavus. J Pediatr Hematol Oncol. 2020 Jul;42(5):350-358. doi: 10.1097/MPH.0000000000001845. PMID: 32576782. 50. Tebbi CK, Badiga A, Sahakian E, Powers JJ, Achille AN, Patel S, Migone F. Exposure to a mycovirus containing Aspergillus Flavus reproduces acute lymphoblastic leukemia cell surface and genetic markers in cells from patients in remission and not controls. Cancer Treat Res Commun. 2021;26:100279. doi: 10.1016/j.ctarc.2020.100279. Epub 2020 Dec 11. PMID: 33348275.
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Further reading
- Boine, Barbara (2012). A study of the interaction between the plant pathogenic fungus Botrytis cinerea and the filamentous ssRNA mycoviruses Botrytis virus X and Botrytis virus F (PhD thesis). The University of Auckland, School of Biological Sciences, Plant and Fungal Virology.
External links
- Media related to Mycoviruses at Wikimedia Commons
- "International Committee on Taxonomy of Viruses".