Alfalfa mosaic virus

Alfalfa mosaic virus (AMV), also known as Lucerne mosaic virus or Potato calico virus, is a worldwide distributed phytopathogen that can lead to necrosis and yellow mosaics on a large variety of plant species, including commercially important crops. It is the only Alfamovirus of the Bromoviridae family. In 1931 Weimer J.L. was the first to report AMV in alfalfa (Medicago sativa). Transmission of the virus occurs mainly by some aphids (plant lice), by seeds or by pollen to the seed.[1] [2]

Alfalfa mosaic virus
Alfamovirus on clover
Virus classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Alsuviricetes
Order: Martellivirales
Family: Bromoviridae
Genus: Alfamovirus
Species:
Alfalfa mosaic virus

Structure and genome

The virion has a capsid (coat protein) but no envelope. The icosahedral symmetry of the capsid is round to elongated. The range for the length of the virion particle is about 30–57 nm. AMV is a multipartite virus and is composed of 4 particles (3 bacilliform and 1 spheroidal) with a diameter of 18 nm.[3] [4] The genetic material of AMV consists of 3 linear single strands RNAs (RNA 1, RNA 2 and RNA 3) and a subgenomic RNA (RNA 4) which is obtained by transcription of the negative- sense strand of RNA 3. RNA 1 and 2 encode proteins needed for replication. RNA 3 is required for the synthesis of the protein responsible for cell-to-cell movement. RNA 4 encodes the capsid. Beside encapsidation and its role in movement the viral coat protein also plays a role in the initiation of RNA replication. This property is called genome activation and means that the genomic nucleic acid is not infectious without the capsid. Specific association of the coat protein with the RNA 3’- terminal sequences or with the subgenomic mRNA is required for the infection. Bacilliform particles contain separately encapsidated RNAs 1, 2 and 3. Spheroidal particles each have two copies of RNA 4. The nucleotide sequence of the complete genome has been determined and the length of the genome is 8274 nucleotides ( or 9155 including the subgenomic RNA). RNA 1, 2, 3 and 4 are respectively 3644 (3.65kb), 2593 (2.6kb), 2037 (2.2kb) and 881 (0.88kb) nucleotides long.[5] [6] [7]

Replication cycle

The AMV cycle can be split up in 5 steps:

  • 1st step: AMV enters the cell and the particles disassemble. The capsid protein remains attached to the coat protein binding site (CPB) at the 3’- end of the RNAs. The initiation factors elF4A, elF4E and elF4G of the host bind to the cap (5’-end).
  • 2nd step: The coat protein interacts with an initiation factor. This triggers translation of RNA1 and 2 into replicase proteins P1 and P2. The complex P1/P2 binds to the RNA.
  • 3rd step: Targeting of RNA to the tonoplast by P1/P2. The capsid dissociates from CPB. CPB undergoes a conformational change into TLS (tRNA-like structure). P1/P2 bind to the minus- strand promoter which is made up of TLS and hairpin E (directs initiation of some transcriptions).
  • 4th step: Minus- strand RNAs are synthesized.
  • 5th step: Plus- strand RNAs and viral proteins are synthesized. Virions assemble.

(Most details of the replication cycle are still unknown).[8]

Pathology

AMV infects over 600 plant species in 70 families (experimental and natural hosts). Some hosts: potato (Solanum tuberosum), pea (Pisum sativum), tobacco (Nicotiana tabacum), tomato (Lycopersicon esculentum), bluebeard (Caryopteris incana), ...

Symptoms vary from wilting, white flecks, malformation like dwarfing, ringspots, mottles, mosaics to necrosis depending on the virus strain, host variety, stage of growth at infection and environmental conditions. Signs of infection can persist or disappear quickly. The virus can be detected in each part of the host plant. The virions are mainly found in the cytoplasm of the infected plant (as inclusion bodies).

Inclusions of Alfalfa mosaic virus

In vitro AMV has a longevity of 1–4 days (sometimes much longer). Temperature and light are the environmental factors that have the greatest influence on the multiplication and movement of AMV in the plant and thus indirectly on the symptoms. Under low temperature the appearance of necrosis for example is less than that for high temperature. The virus usually reaches his inactivation temperature at 60–65 °C. Dark conditions slow down the virus multiplication, while light speeds it up. A hypothesis for this phenomenon is that shading causes a decrease in ATP production by photosynthesis. The optimum pH was found to be about pH 7–7.5 for AMV in sap (depending on the host species). It has been proved that in the important forage grass alfalfa, the infection by AMV leads to a decrease of Cu, Fe, Mn, P and Zn quantities. On the other hand, an increase in N (viral protein) was observed. Infected alfalfa was also not seen to be harmful for domestic animals.[9] [10] [11] [12]

AMV is a very variable plant virus and several strains with minor differences exist (strain Q, strain S, strain 425, strain AlMV-B, strain AlMV- S,...). Distinction is based on different symptoms in one or two chosen hosts and also on, for example, differential physico-chemical properties.[13]

Transmission

The vectors are insects of the order Hemiptera, family Aphididae; green peach aphids (Myzus persicae) and at least 14 other species are known to play that role. AMV can also be transmitted by seed, pollen, through mechanical inoculation of plant sap and by the parasitic plant dodder (Cuscuta). The combination of seed-infected plants and spreading by aphids results mostly in high levels of infection.

Economic importance

The host range of the virus is wide and includes food and pasture crops (peas, lentils, potatoes, clovers,…). Infection by AMV causes important yield losses, reduces winter survival and facilitates infection of the affected plant by other pathogens.[14]

Management

Insecticides against aphids are not effective for controlling AMV. Recommendations are sowing healthy seed (some seed companies sell seed tested for AMV), managing weeds, avoiding growing crops adjacent to infected pasture and other cultural practices to minimize AMV.[15] Work has been done on creating transgenic AMV resistant plants. For example, DNA derived from AMV encoding the gene for the capsid has been inserted into alfalfa plants. This reduced the susceptibility of the plants to infection by AMV and the plants would be less of a reservoir of virus for spread to other plants.[16]

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See also

References
  1. ICTVdB Management (2006). "Alfalfa mosaic virus". In: ICTVdB—The Universal Virus Database, version 4. Büchen-Osmond, C. (Ed), Columbia University, New York, USA.
  2. Bisby FA, Roskov YR, Orrell TM, Nicolson D, Paglinawan LE, Bailly N, Kirk PM, Bourgoin T, van Hertum J, eds. (2008). "Species 2000 & ITIS Catalogue of Life: 2008 Annual Checklist". Reading, U.K.
  3. Agrios G. N. (1997). Plant pathology. San Diego, Academic Press, 635 p.
  4. Kumar A.; Reddy V. S.; Yusibov V.; Chipman P. R.; Hata Y.; Fita I.; Fukuyama K.; Rossmann M. G.; Loesch-Fries L. S.; Baker T. S.; Johnson J. E. (1997). "The structure of alfalfa mosaic virus capsid protein assembled as T=1 icosahedral particle at 4.0-Å resolution" (PDF). Journal of Virology. 71 (10): 7911–7916. doi:10.1128/JVI.71.10.7911-7916.1997.
  5. Laforest S.M.; Gehrke L. (2004). "Spatial determinants of the alfalfa mosaic virus coat protein binding site". RNA. 10 (1): 48–58. doi:10.1261/rna.5154104. PMC 1370517. PMID 14681584.
  6. Tenllado F.; Bol J. (2000). "Genetic dissection of the multiple functions of alfalfa mosaic virus coat protein in viral RNA replication, encapsidation, and movement". Virology. 268 (1): 29–40. doi:10.1006/viro.1999.0170. PMID 10683324.
  7. Yusibov V.; Kumar A.; North A.; Johnson J.E.; Loesch-Fries L.S. (1996). "Purification, characterization, assembly and crystallization of assembled alfalfa mosaic virus coat protein expressed in Escherichia coli" (PDF). Journal of General Virology. 77 (4): 567–573. doi:10.1099/0022-1317-77-4-567. PMID 8627243.
  8. Bol J.F. (2003). "Alfalfa mosaic virus: coat protein-dependent initiation of infection". Molecular Plant Pathology. 4 (1): 1–8. doi:10.1046/j.1364-3703.2003.00146.x. PMID 20569357.
  9. Kudo A.; Misawa T. (1971). "Some phenoma observed in systemic infection of alfalfa mosaic virus: the influences of air temperature and shading on symptom appearance". Tohoku Journal of Agricultural Research. 22: 199–206.
  10. Alblas F.; Bol J.F. (1977). "Factors influencing the infection of cowpea mesophyll protoplasts by alfalfa mosaic virus" (PDF). J. Gen. Virol. 36: 175–185. doi:10.1099/0022-1317-36-1-175.
  11. Yardımcı N; Eryiğit H.; Erdal I (2006–2007). "Effect of alfalfa mosaic virus (AMV) on the content of some macro- and micronutrients in alfalfa" (PDF). Journal of Culture Collections. 5: 90–93.
  12. Jaspars E.M.J.; Bos L. (1980). "Alfalfa mosaic virus". AAB Descriptions of Plant Viruses.
  13. Hyo Won Jung; Hye Jin Jung; Wan Soo Yun; Hye Ja Kim; Young ll Hahm; Kook-Hyung Kim; Jang Kyung Choi (2000). "Characterization and partial nucleotide sequence analysis of alfalfa mosaic alfamoviruses isolated from potato and azuki bean in Korea" (PDF). Plant Pathology Journal. 16 (5): 269–279.
  14. McDonald J. G.; Suzuki M. (1983). "Occurrence of alfalfa mosaic virus in Prince Edward Island" (PDF). Canadian Plant Disease Survey. 63: 47–50.
  15. Freeman A.; Aftab M. (2006). "Temperature pulse viruses: alfalfa mosaic virus (AMV)". Agriculture Notes: 1–3.
  16. Spangenberg G. (2001). Molecular breeding of forage crops. Victoria, Springer, 356 p.
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