Plum pox virus (sharka)
- Summary of Invasiveness
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Habitat List
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Latitude/Altitude Ranges
- Air Temperature
- Rainfall Regime
- Means of Movement and Dispersal
- Seedborne Aspects
- Pathway Causes
- Pathway Vectors
- Plant Trade
- Vectors and Intermediate Hosts
- Impact Summary
- Economic Impact
- Environmental Impact
- Social Impact
- Risk and Impact Factors
- Detection and Inspection
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Plum pox virus
Preferred Common Name
Other Scientific Names
- Annulus pruni
- plum pox potyvirus
- Prunus virus 7
- Sharka virus
International Common Names
- English: peach sharka; pox disease of plum; sharka disease of plum
- French: variole du prunier
Local Common Names
- Germany: Aprikose; Aprikose, Pfirsich Scharka-Virus: Pflaume; Pfirsich Scharka-Virus; Scharka-Krankheit; scharkakrankheit der pflaume
- Italy: Vaiolatura delle drupacee; Vaiolatura delle drupacee
- PPV000 (Plum pox potyvirus)
Summary of InvasivenessTop of page
Plum pox virus disease (Sharka) is one of the most destructive diseases of stone fruits. The causal agent, Plum pox virus (PPV) is easily transmitted by many aphid species in a non-persistent manner, by manmade grafting (nursery trade), and has a very wide host range among Prunus species. Infected plants may not show symptoms for several months and symptoms are often transient in appearance. The disease symptoms are often mistaken for other maladies and the virus can become established before the first recognition of the disease. Although spread is difficult to control within a local area because of aphid vectors, the long distance spread can be controlled by strict quarantine regulations and use of virus-free certified nursery stock.
Taxonomic TreeTop of page
- Domain: Virus
- Unknown: "Positive sense ssRNA viruses"
- Unknown: "RNA viruses"
- Family: Potyviridae
- Genus: Potyvirus
- Species: Plum pox virus
Notes on Taxonomy and NomenclatureTop of page
Strains of Plum pox virus (PPV) were originally distinguished (necrotic, intermediate, yellow) on the basis of symptoms induced in herbaceous indicator plants. Kerlan and Dunez (1979) then serologically differentiated D (Dideron) and M (Markus) types, the former on apricot (Prunus armeniaca) in France and the latter originally on peach (Prunus persica) in Greece. Bousalem et al. (1994) have examined 28 PPV isolates from 11 countries and found that they could be consistently grouped into two major types (D and M) using three techniques: electrophoretic mobility of coat protein; antigenic properties of the N and C regions of coat protein; and the presence of a specific restriction site in the C-terminal region of the coat protein.
The El Amar strain from Egypt is distinct from the other two strains on the basis of divergences in RNA sequence (Wetzel et al., 1991a). The cherry strain, termed PPV-C (Cherry), has been found to infect sweet (Prunus avium) and sour cherry trees (Prunus cerasus) in Italy, Moldova, Bulgaria and Hungary (Crescenzi et al., 1994, 1995, 1997; Kalashyan et al., 1994; Kölber et al., 1998; Nemchinov and Hadidi, 1996; Nemchinov et al., 1995, 1996, 1998a, c; Topchiiska, 1991, 1996). This strain is significantly different from other strains of PPV in biological, serological and molecular properties.
A fifth strain of PPV, termed PPV-W (W3174 - Winona), was identified in Canada (James et al., 2003; James and Varga, 2005). The plant containing this strain was destroyed. A sixth strain of PPV termed PPV-Rec, is a stable recombinant consisting of D and M strain recombinants with a common phylogenetic link (Glasa et al., 2002, 2004). It has been reported from several European countries, many times having been incorrectly identified as PPV-M. Within these strains, individual isolates can vary in the severity of symptoms they induce. For example, a strain of the M type was reported from France in the 1980s, which is very aggressive and necrogenic on peach (Candresse et al., 1993). The necrogenic strain involved has been referred to as PPV-SP and was further characterized by Adamolle et al. (1994). Currently, PPV is divided into six subgroups or serotypes or strains: PPV-D, PPV-M, PPV-El Amar, PPV-C, PPV-W, and PPV-Rec (Candresse and Cambra, 2006; James and Glasa, 2006).
A virus that infects Prunus spp. in eastern Asia and named Asian prunus latent virus (APLV) has been reported to cross react with PPV antiserum (Hadidi and Levy, 1994; Hari et al., 1995; James et al., 1996). This virus was detected in North America in quarantined peach and Prunus mume (Japanese apricot) germplasm imported from eastern Asia. It can be distinguished from PPV using certain specific DNA primers, but cross-reacts in other tests.
Similarly, another virus in Moldova that infects stone fruits, Apricot latent virus (ALV), has recently been reported to cross-react with PPV antiserum, but can be distinguished from PPV in PCR and other assays (Nemchinov and Hadidi, 1998b). The exact taxonomy of APLV and ALV is presently undetermined.
DescriptionTop of page
PPV has filamentous virus particles 750 nm long and 15 nm in diameter. It has a single-stranded RNA genome with a MW of 3.5 x 106 Da. Protein inclusions, of the pinwheel type, are present in the cytoplasm of infected cells (Salvador et al., 2006).
Different RNAs from PPV have been cloned (Ravelonandro et al., 1988a) and the complete or partial nucleotide sequences of several virus isolates have been determined (Maiss et al., 1989; Teycheney et al., 1989; Wetzel et al., 1991a; Cervera et al., 1993; Garcia et al., 1994; Nemchinov et al., 1996, 1998b). Recently several additional sequences have been submitted to Genbank (National Center for Biotechnology Information: http://www.ncbi.nlm.nih.gov/). Sequence differences among PPV strains have been detected and seem to be spread in a uniform manner on the genome (Palkovics et al., 1995). Genome function in PPV is now increasingly understood, and this virus is now a model for studies on the molecular biology of potyviruses (García et al., 1994).
DistributionTop of page
PPV was first detected in eastern Europe (Bulgaria) (Atanassov, 1932) from where it has spread to most countries of the continent (OEPP/EPPO, 2006). Until 1992, no occurrence had been reported from outside the Euro-Mediterranean area. A report on finding PPV in India (Thakur et al., 1994) has not yet been confirmed. PPV was detected in Chile in 1992 (Herrera, 1994; Rosales et al., 1998), the USA in 1999 (Levy et al., 2000; ProMED, 2006; Snover-Clift et al., 2007), Canada in 2000 (Thompson et al., 2001), China in 2004 (Navratil et al., 2005) and Argentina in 2005 (Dal Zotto et al., 2006).
PPV is present or has occurred in almost all European countries to varying degrees. Roy and Smith (1994) distinguished three zones: the central and eastern countries in which PPV spread relatively early and infection levels are generally high (Bosnia-Herzegovina, Bulgaria, Croatia, Czech Republic, Hungary, Moldova, Poland, Romania, Serbia, Slovakia, Slovenia, Ukraine); the Mediterranean countries in which spread is more recent and there is a high risk of further spread (Albania, Cyprus, Egypt, Greece, Italy, Portugal, Spain, Syria, Turkey); and the northern and western countries in which levels of PPV are very uneven (fairly widespread in Austria, Germany and the UK (England)), very localized in Belgium and Luxembourg, localized in France, transient and under eradication in Denmark, and few occurrences in Netherlands and Switzerland. PPV has been found in several areas of Russia although mainly in botanical gardens, research institutions and a few farms. (See CABI/EPPO Distribution Maps of Plant Diseases: 1998, 1999, 2007.)
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Azerbaijan||Absent, unreliable record||EPPO, 2014|
|China||Present, few occurrences||Introduced||2005||Not invasive||Navratil et al., 2005; CABI/EPPO, 2007; EPPO, 2014|
|-Hunan||Present, few occurrences||CABI/EPPO, 2007; EPPO, 2014|
|Georgia (Republic of)||Absent, formerly present||EPPO, 2014|
|India||Restricted distribution||Introduced||1995||CABI/EPPO, 2007; EPPO, 2014|
|-Himachal Pradesh||Present||Introduced||1994||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Iran||Present||Introduced||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Israel||Present, few occurrences||EPPO, 2014; EPPO, 2014|
|Japan||Present, few occurrences||EPPO, 2011; EPPO, 2014|
|-Honshu||Present, few occurrences||EPPO, 2014; Oishi et al., 2018|
|Jordan||Present, few occurrences||Introduced||2000||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Kazakhstan||Present||Introduced||2004||Not invasive||Spiegel et al., 2004; CABI/EPPO, 2007; EPPO, 2014|
|Korea, Republic of||Present||Oh et al., 2017||Strain D isolate in peach.|
|Lebanon||Absent, confirmed by survey||EPPO, 2014|
|Pakistan||Restricted distribution||Introduced||2006||Not invasive||Kollerová et al., 2006; CABI/EPPO, 2007; EPPO, 2014|
|Syria||Present, few occurrences||Introduced||1988||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Turkey||Restricted distribution||Introduced||1968||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; Akbas et al., 2011; EPPO, 2014|
|Egypt||Widespread||Introduced||1986||Not invasive||Mazyad et al., 1992; Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Tunisia||Present, few occurrences||Introduced||2000s||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Canada||Restricted distribution||Introduced||2001||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|-Nova Scotia||Eradicated||CABI/EPPO, 2007; EPPO, 2014|
|-Ontario||Restricted distribution||Introduced||2001||CABI/EPPO, 2007; EPPO, 2014|
|USA||Present, few occurrences||CABI/EPPO, 2007; EPPO, 2014|
|-Michigan||Eradicated||2009||CABI/EPPO, 2007; NAPPO, 2009; EPPO, 2014|
|-New York||Restricted distribution||Introduced||2006||Not invasive||CABI/EPPO, 2007; Snover-Clift et al., 2007; NAPPO, 2013; EPPO, 2014; NAPPO, 2016|
|-Pennsylvania||Eradicated||2009||Levy et al., 2000; CABI/EPPO, 2007; NAPPO, 2009; EPPO, 2014|
|Argentina||Present, few occurrences||2004||Not invasive||Dal Zotto et al., 2006; CABI/EPPO, 2007; EPPO, 2014|
|Chile||Widespread||1992||Roy and Smith, 1994; Herrera et al., 1998; Rosales et al., 1998; CABI/EPPO, 2007; EPPO, 2014|
|Albania||Widespread||Introduced||1971||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014; Palmisano et al., 2015|
|Austria||Restricted distribution||1961||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Belgium||Present, few occurrences||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Bosnia-Hercegovina||Present||Introduced||1960s||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Bulgaria||Widespread||Introduced||1915||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Croatia||Widespread||Introduced||1960s||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Cyprus||Widespread||Introduced||1982||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Czech Republic||Widespread||Introduced||1940s||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Denmark||Transient: actionable, under eradication||Introduced||1986||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2011; IPPC, 2011; EPPO, 2014|
|Estonia||Absent, formerly present||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Finland||Present||Santala and Soukainen, 2015|
|France||Restricted distribution||Introduced||1970||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014; Svanella-Dumas et al., 2015|
|-France (mainland)||Restricted distribution||CABI/EPPO, 2007|
|Germany||Widespread||Introduced||1960s||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Greece||Widespread||Introduced||1967||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|-Greece (mainland)||Widespread||CABI/EPPO, 2007|
|Hungary||Widespread||Introduced||1948||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Italy||Restricted distribution||Introduced||1973||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|-Italy (mainland)||Restricted distribution||CABI/EPPO, 2007|
|-Sicily||Present||Rizza et al., 2014|
|Latvia||Present, few occurrences||IPPC, 2009a; IPPC, 2009b; EPPO, 2014|
|Lithuania||Present, few occurrences||Introduced||1995||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Luxembourg||Present||Introduced||1961||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Moldova||Restricted distribution||Introduced||1960s||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Montenegro||Widespread||CABI/EPPO, 2007; EPPO, 2014|
|Netherlands||Present, few occurrences||Introduced||1965||Not invasive||NPPO of the Netherlands, 2013; CABI/EPPO, 2007; EPPO, 2014|
|Norway||Restricted distribution||Introduced||1998||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Poland||Widespread||Introduced||1962||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Portugal||Restricted distribution||Introduced||1984||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|-Azores||Present||Introduced||1996||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|-Portugal (mainland)||Restricted distribution||CABI/EPPO, 2007|
|Romania||Widespread||Introduced||1941||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Russian Federation||Restricted distribution||Introduced||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|-Central Russia||Present||Introduced||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|-Southern Russia||Restricted distribution||Introduced||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|Serbia||Widespread||Introduced||1935||Not invasive||CABI/EPPO, 2007; Marn et al., 2008; EPPO, 2014|
|Slovakia||Widespread||Introduced||1950||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Slovenia||Restricted distribution||Introduced||1987||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Spain||Restricted distribution||Introduced||1981||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|-Spain (mainland)||Restricted distribution||CABI/EPPO, 2007|
|Sweden||Absent, intercepted only||CABI/EPPO, 2007; EPPO, 2014|
|Switzerland||Present, few occurrences||Introduced||1967||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|UK||Restricted distribution||Introduced||1965||Not invasive||CABI/EPPO, 2007; EPPO, 2014|
|-England and Wales||Restricted distribution||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|Ukraine||Restricted distribution||Introduced||1967||Not invasive||Roy and Smith, 1994; CABI/EPPO, 2007; EPPO, 2014|
|New Zealand||Absent, confirmed by survey||EPPO, 2014|
Risk of IntroductionTop of page Introduction can be accidental or intentional by bringing in what appears to be symptomless budwood for grafting. Symptoms do not appear for several months leading to establishment of the disease before obvious symptoms appear.
Habitat ListTop of page
|Terrestrial – Managed||Cultivated / agricultural land||Principal habitat||Harmful (pest or invasive)|
|Urban / peri-urban areas||Principal habitat|
Hosts/Species AffectedTop of page
The main woody hosts are the fruit-producing species of Prunus, including apricots (Prunus armeniaca), peaches (Prunus persica) and plums (Prunusdomestica, Prunussalicina and Prunuscerasifera). Almonds (Prunusdulcis) can be infected with PPV, but show few, if any, natural symptoms (Festic, 1978; Llácer and Cambra, 2006). Almond trees in Chile were naturally infected with PPV (Herrera et al., 1998), but similar surveys in France failed to demonstrate natural infection by PPV in almond. Isolates of the D and M serotypes were transmitted experimentally to different cherry species, but infection remained localized and the virus was not shown to be translocated (Dosba et al., 1987). However, a Pennsylvanian isolate of PPV was transmitted to several ornamental flowering cherries and sweet cherry (Prunus avium) by aphids and grafting, with symptom development and subsequent back-transfer to peach (Damsteegt et al., 2007).
Natural infections of Prunus cerasus (sour cherry) and P. avium with PPV-C in four European countries have been reported (Crescenzi et al., 1994, 1995, 1997; Nemchinov and Hadidi, 1996; Nemchinov et al., 1996, 1998a, c). PPV-C has been transmitted by grafting or vectors to other stone fruit species (Kalashyan et al., 1994; Nemchinov et al., 1996, 1998c; Crescenzi et al., 1997).
Most wild or ornamental species of Prunus can be experimentally infected by PPV-D through aphid feeding and grafting (Damsteegt et al., 2007).
Natural secondary hosts
Prunus spinosa (blackthorn) was long considered to be a natural host of PPV. Results obtained in the former Yugoslavia did not confirm this (Rankovic and Dulic-Markovic, 1992); however, it has been shown to be a systemic host in France (Labonne et al., 2004) and the Czech Republic (Polak, 2004). In addition, Polak (2001) reported natural infection in Ligustrum vulgare (European privet) and Euonymus europaea (European spindletree). Other reported natural hosts are P. avium, Prunus besseyi (bessey cherry), P. cerasifera (myrobalan plum), Prunus tomentosa (Nanking cherry tree), Prunus glandulosa (flowering almond), Prunus japonica (Japanese bush cherry tree), Prunus serotina (black cherry) and Prunus x blireiana (prunier double) (James and Thompson, 2006).
Susceptible Prunus spp. are widely grown for fruit production (varieties and rootstocks) worldwide and throughout all European parts of the EPPO region. Wild woody and herbaceous hosts are widespread and are potential reservoirs of the pathogen, although a direct contribution of these hosts to the epidemiology of PPV has never been clearly demonstrated. Numerous cultivated or weedy annual plants have been shown to be experimental and natural hosts of PPV (Nemeth, 1986; Milusheva and Rankova, 2002; Viršcek et al., 2004; Llácer, 2006).
Host Plants and Other Plants AffectedTop of page
|Cichorium (chicory)||Asteraceae||Wild host|
|Cirsium arvense (creeping thistle)||Asteraceae||Wild host|
|Convolvulus arvensis (bindweed)||Convolvulaceae||Wild host|
|Juglans regia (walnut)||Juglandaceae||Other|
|Ligustrum vulgare (common privet)||Oleaceae||Other|
|Prunus americana (American plum)||Rosaceae||Main|
|Prunus angustifolia (Mountain cherry tree)||Rosaceae||Main|
|Prunus armeniaca (apricot)||Rosaceae||Main|
|Prunus avium (sweet cherry)||Rosaceae||Other|
|Prunus besseyi (bessey cherry)||Rosaceae||Other|
|Prunus cerasifera (myrobalan plum)||Rosaceae||Other|
|Prunus domestica (plum)||Rosaceae||Main|
|Prunus dulcis (almond)||Rosaceae||Main|
|Prunus emarginata (Bitter cherry tree)||Rosaceae||Main|
|Prunus fruticosa (dwarf cherry)||Rosaceae||Main|
|Prunus glandulosa (flowering almond)||Rosaceae||Wild host|
|Prunus ilicifolia (holly-leaved cherry)||Main|
|Prunus japonica (Japanese bush cherry tree)||Rosaceae||Wild host|
|Prunus mahaleb (mahaleb cherry)||Rosaceae||Main|
|Prunus maritima (beach plum)||Rosaceae||Main|
|Prunus nigra (Canada plumtree)||Rosaceae||Main|
|Prunus padus (bird cherry)||Rosaceae||Main|
|Prunus pensylvanica (pin cherry)||Rosaceae||Main|
|Prunus persica (peach)||Rosaceae||Main|
|Prunus pumila var. besseyi||Rosaceae||Main|
|Prunus pumila var. depressa||Rosaceae||Main|
|Prunus salicina (Japanese plum)||Rosaceae||Main|
|Prunus sargentii (sargent's cherry)||Rosaceae||Main|
|Prunus serotina (black cherry)||Rosaceae||Unknown|
|Prunus serrulata (Japanese flowering cherry)||Rosaceae||Main|
|Prunus spinosa (blackthorn)||Rosaceae||Other|
|Prunus subhirtella (weeping Japanese cherry)||Rosaceae||Main|
|Prunus tomentosa (Nanking cherry tree)||Rosaceae||Main|
|Prunus triloba (Rose tree of China)||Rosaceae||Main|
|Prunus virginiana (common chokecherrytree)||Rosaceae||Main|
|Prunus virginiana var. demissa||Rosaceae||Main|
|Rorippa sylvestris (creeping yellowcress)||Brassicaceae||Wild host|
|Solanum nigrum (black nightshade)||Solanaceae||Wild host|
|Taraxacum officinale complex (dandelion)||Asteraceae||Wild host|
|Trifolium (clovers)||Fabaceae||Wild host|
Growth StagesTop of page Flowering stage, Fruiting stage, Vegetative growing stage
SymptomsTop of page
Symptoms may appear on leaves or fruits. They are particularly conspicuous on leaves in spring: chlorotic spots, bands or rings, vein clearing, or even leaf deformation in peaches. Some peach cultivars may also show flower breaking symptoms. Infected fruits show chlorotic spots or rings.
Diseased plums and apricots are deformed and show internal browning of the flesh; apricot stones show pale rings or spots (Dunez, 1987). Symptoms of sharka depend very much on the locality, the season, Prunus species and cultivar, and plant tissue (leaf or fruit) (Dosba et al., 1986; Kegler and Hartmann, 1998; Nemchinov et al., 1998a).
List of Symptoms/SignsTop of page
|Fruit / abnormal shape|
|Fruit / lesions: black or brown|
|Fruit / premature drop|
|Leaves / abnormal colours|
|Leaves / abnormal forms|
|Leaves / abnormal patterns|
|Seeds / discolorations|
|Stems / dieback|
Biology and EcologyTop of page
Infected Prunus trees are the major source of inoculum. The virus is transmitted from infected trees either by grafting or, non-persistently, by aphid vectors such as Aphisspiraecola and Myzus persicae. Other aphid species have been shown to transmit at a lower frequency than the two main vectors: Aphis craccivora, Aphis fabae, Brachycauduscardui, Brachycaudus helychrysi, Brachycaudus persicae, Hyalopterus pruni,Myzus varians and Phorodonhumuli (Kunze and Krczal, 1971; Leclant, 1973). Avinent et al. (1994) have recently added Aphis gossypii to the list of minor PPV vectors in Spain, whilst in France, Labonne et al. (1994) have shown that this species as well as Aphis hederae and Rhopalosiphumpadi transmitted PPV to an herbaceous host. Gildow et al. (2004) added Metopolophium dirhodum (rose-grain aphid) and Toxoptera citricida (brown citrus aphid) as vectors of PPV under experimental conditions.
The number of trees becoming infected in an orchard is directly related, in a given season, to numbers of winged aphids. These aphids probe or feed on infected leaves, then fly to other trees where they again probe or feed. Gottwald et al. (1995), after analyzing the spatial distribution of aphid-borne spread in eastern Spain, concluded that aphids spread the disease to trees several spaces away rather than to immediately adjacent trees.
In summer, the aphids may also migrate to various herbaceous species present in orchards and return to the fruit trees to lay their winter eggs (Kunze and Krczal, 1971). Phorodon humuli, after fasting, has been shown to be capable of spreading PPV over long distances, 2-3 h after acquisition (Krczal and Kunze, 1972). The capacity for vector transmission varies considerably between strains (Massonié and Maison, 1976). After inoculation, the incubation period may last several months and systemic spread within woody hosts may take several years (OEPP/EPPO, 1983). Accordingly, the virus may be distributed very irregularly in the tree.
Németh and Kölber (1983) reported seed transmission in Prunus, but this has not been confirmed by other workers during the last 15 years, and is unknown in practice. Other researchers have failed to find evidence of seed transmission of PPV in Prunus (Pasquini and Barba, 2006).
Labonne and Quiot (2001) were the first to describe transmission of PPV-M and PPV-D by M. persicae from infected apricot (Prunus armeniaca) and peach (Prunus persica) fruit. Gildow et al. (2004) found M. persicae and Aphis spiraecola could transmit PPV-D from symptomatic and asymptomatic peach fruit.
ClimateTop of page
|C - Temperate/Mesothermal climate||Preferred||Average temp. of coldest month > 0°C and < 18°C, mean warmest month > 10°C|
|Cf - Warm temperate climate, wet all year||Tolerated||Warm average temp. > 10°C, Cold average temp. > 0°C, wet all year|
Latitude/Altitude RangesTop of page
|Latitude North (°N)||Latitude South (°S)||Altitude Lower (m)||Altitude Upper (m)|
Air TemperatureTop of page
|Parameter||Lower limit||Upper limit|
|Mean maximum temperature of hottest month (ºC)||30||40|
|Mean minimum temperature of coldest month (ºC)||-25||0|
RainfallTop of page
|Parameter||Lower limit||Upper limit||Description|
|Dry season duration||1||2||number of consecutive months with <40 mm rainfall|
|Mean annual rainfall||0||900||mm; lower/upper limits|
Rainfall RegimeTop of page Uniform
Means of Movement and DispersalTop of page
There are no known means of natural dispersal. Dispersal is either via human transport of infected plant parts or via aphid vectors.
This is by several species of aphids in a non-persistent manner. Aphids can acquire the virus from infected leaves, flowers, or fruits in very short time periods (seconds to minutes) and can transmit it to new plants within a few minutes. There is no latent period in the insect.
The disease appears randomly in orchards. After 2-3 years (possibly sooner in peach orchards), infection begins to spread from the first infected trees (Llácer et al., 1986). Graft transmission can contribute significantly to spread in infected areas if certified virus-free material is not used. Dissemination of the virus between areas or countries is most often in uncertified planting material (Diekmann and Putter, 1996).
PPV is occasionally intercepted in fruit-tree material imported into the USA from eastern Europe (Waterworth, 1994). PPV contaminated anthers could potentially play a role in PPV dissemination at the national and international levels (Levy et al., 1995) because the virus is present in these organs. However, this possibility has never been documented in practice.
Seedborne AspectsTop of page
PPV has been detected in seed coats and cotyledons, but embryonic tissue and seedlings obtained from germinated seeds never showed symptoms, and gave negative results for PPV with both ELISA and PCR assays. No PPV isolate is currently recognized to be seed transmitted, so vertical transmission of PPV from infected mother plants to their progeny does not occur (Paquini and Barba, 2006).
Pathway CausesTop of page
Pathway VectorsTop of page
Plant TradeTop of page
|Plant parts liable to carry the pest in trade/transport||Pest stages||Borne internally||Borne externally||Visibility of pest or symptoms|
|Fruits (inc. pods)||adults||Yes||Pest or symptoms usually visible to the naked eye|
|Leaves||adults; nymphs||Yes||Pest or symptoms usually visible to the naked eye|
|Roots||Yes||Pest or symptoms usually invisible|
|Seedlings/Micropropagated plants||adults; nymphs||Yes||Pest or symptoms usually visible to the naked eye|
|Stems (above ground)/Shoots/Trunks/Branches||adults; nymphs||Yes||Pest or symptoms usually visible to the naked eye|
|Plant parts not known to carry the pest in trade/transport|
|Growing medium accompanying plants|
|True seeds (inc. grain)|
Vectors and Intermediate HostsTop of page
|Aphis craccivora||Glasa and Candresse, 2005.||Insect|
|Aphis gossypii||Glasa and Candresse, 2005.||Insect|
|Aphis hederae||Glasa and Candresse, 2005.||Insect|
|Aphis spiraecola||Glasa and Candresse, 2005.||Insect|
|Brachycaudus cardui||Glasa and Candresse, 2005.||Insect|
|Brachycaudus helichrysi||Glasa and Candresse, 2005.||Insect|
|Brachycaudus persicae||Glasa and Candresse, 2005.||Insect|
|Metopolophium dirhodum||Gildow et al., 2004.||Insect|
|Myzus persicae||Glasa and Candresse, 2005.||Insect|
|Myzus varians||Glasa and Candresse, 2005.||Insect|
|Phorodon humuli||Glasa and Candresse, 2005.||Insect|
|Rhopalosiphum padi||Glasa and Candresse, 2005.||Insect|
Impact SummaryTop of page
|Human health||Positive and negative|
ImpactTop of page
Economic ImpactTop of page
PPV is an EPPO A2 quarantine pest (OEPP/EPPO, 1983, 1990, 2004). It is also considered to be a quarantine pest by IAPSC and NAPPO (Foster and Hadidi, 1998; Thompson, 1998). In the EPPO region, it presents a major risk to apricots (Prunus armeniaca), plums and peaches (Prunus persica) in many countries where it is still absent or very localized (Diekmann and Putter, 1996). In addition, its presence in a country creates difficulties for the export of certified planting material. An EPPO quarantine procedure for PPV has been prepared (OEPP/EPPO, 1992).
Németh (1994), Kegler and Hartmann (1998) and Nemchinov et al. (1998a) have reviewed the importance of plum pox on European stone-fruit production. Sharka disease is particularly serious in the fruit-producing areas of central and eastern Europe. During the past decade, it has progressively spread to some Mediterranean countries such as Egypt (Wetzel et al., 1991a; Mazyad et al., 1992), Spain (Llácer et al., 1985) and Portugal (Louro and Monte Corvo, 1986). It has also been reported from Chile (Herrera et al., 1998). Virus infection can lead to considerable yield losses, reaching 83-100% in highly susceptible varieties (Kegler and Hartmann, 1998; Nemchinov et al., 1998a; Waterworth and Hadidi, 1998). European plums (Prunus domestica) may show premature fruit drop, while Japanese plums (Prunus salicina) and peaches show ring spotting on fruit, and apricots show serious fruit deformation. The disease impact is, however, modulated to a large extent by the variability in susceptibility/tolerance shown by individual cultivars of its Prunus host species. Sweet cherry (Prunus avium) fruits undergo premature fruit dropping and leaves develop chlorotic and necrotic ring spots or notches (Nemchinov et al., 1998a). An evaluation of the global cost associated with plum pox management worldwide, excluding indirect trade costs, has been estimated at 10,000 million euros (Cambra et al., 2006).
Environmental ImpactTop of page
Because of a loss of value of the trees, orchards are removed much earlier than normal. Often areas are taken out of production of either certain varieties or fruit species that may change the agricultural pattern for a given area.
Social ImpactTop of page
The greatest impact caused by PPV is economic. It does not actually kill trees by itself, but renders the fruit unpalatable. The fruit do not pose a health problem for humans or animals.
Risk and Impact FactorsTop of page Invasiveness
- Invasive in its native range
- Has a broad native range
- Tolerant of shade
- Highly mobile locally
- Host damage
- Negatively impacts agriculture
- Negatively impacts livelihoods
- Pest and disease transmission
- Difficult to identify/detect in the field
- Difficult/costly to control
DiagnosisTop of page
See Cambra et al. (2006) and Olmos et al. (2006) for reviews of serological and molecular methods developed for the detection and characterization of PPV. OEPP (2004) provide a diagnostic protocol standard for PPV.
Vicchi et al. (2005) diagnosed PPV on peach flowers in the field using an immunochromatographic lateral flow (LF) method, which shows similar effectiveness to ELISA.
Detection and InspectionTop of page
In spite of the irregular distribution of the virus in the tree, visual inspection does allow detection by symptoms, especially during the period of active growth, although this method is unreliable with many D strain isolates. Testing on susceptible indicators (peaches (Prunus persica) or downy cherry (Prunus tomentosa)) by chip-budding can produce symptoms in 6-8 weeks (ISHS, 1983, 1992, 1998; OEPP/EPPO, 1983; Damsteegt et al., 1997). Mechanical inoculation to Chenopodium foetidum [Chenopodium schraderianum] or peas (Pisum spp.) results in symptoms in 6-8 days.
Dunez et al. (1994) have reviewed the progress that has been made in detection techniques for PPV. ELISA, which was first applied in plant virology for the detection of PPV, is widely used to confirm the presence of the virus in roots, bark, flowers, leaves, fruits or seeds (Adams, 1978). The method has been applied quantitatively (Himmler et al., 1987).
Methods based on electron microscopy, viz. immuno-electron microscopy (Kerlan et al., 1981) and with colloidal gold staining (Himmler et al., 1988) can also be used. Monoclonal antibodies can be used very effectively, and will distinguish between different strains (M and D types) (Cambra et al., 1994, 2006; Boscia et al., 1997; Candresse et al., 1998). Polyclonal antibodies produced against a peptide, which consists of 14 amino acids of the N-terminal region of PPV-C recognize PPV-C, but not other strains of PPV (Crescenzi et al., 1998).
Molecular hybridization tests based on nucleic acid sequences specifically complementary to virus RNA have been developed. A dot-blot molecular hybridization test using radioactive DNA or RNA probes has been developed by Varveri et al. (1987, 1988). Non-radioactive DIG-labeled PPV cRNA probes have also been developed, some probes differentiate between PPV-C and other strains of PPV (Nemchinov et al., 1996).
Enzymatic amplification of the DNA sequence (by PCR) has increased the sensitivity level of the test to 10 fg of purified viral RNA (Wetzel et al., 1991b). Immunocapture-PCR has been developed as a highly sensitive assay for PPV (Wetzel et al., 1992; Candresse et al., 1994, 1998).
Alternatives to IC-PCR include 'print capture' PCR, which allows viral detection without grinding the sample and with the use of a number of proteins that replace PPV-specific immunoglobins in the capture phase (Olmos et al., 1996, 1998; Cambra et al., 1998; Candresse et al., 1998); and RT-PCR assay specific for the conserved 3' non coding region of PPV, which may utilize GeneReleaser(tm) extraction/purification of nucleic acids (Levy and Hadidi, 1994; Levy et al., 1994). PCR assays specific for PPV strain differentiation have been developed. Candresse et al. (1998) designed two primer pairs that allow the amplification and differentiation of the two major subgroups, D and M, of PPV. In addition, Nemchinov and Hadidi (1998a) have designed primers specific for the amplification of PPV-C. Multiple PCR-based assays have been developed for the detection of PPV in single, quantitative and multiplex formats (James et al., 2003; Mavrodieva and Levy, 2004; Olmos et al., 2004, 2006; Schneider et al., 2004).
Martínez-Gómez et al. (2003) reported that, for the identification of plum pox virus, IC-PCR showed higher sensitivity than ELISA-DASI but was more time-consuming and expensive. Sánchez-Navarro et al. (2005) found multiplex RT-PCR to be more sensitive than ELISA or molecular hybridisation assays at detecting PPV and differentiating it from other viruses that affect stone fruit trees.
Olmos et al. (2007) developed a nucleic acid sequence-based amplification method coupled with rapid flow-through hybridization (NASBA-FH) for the detection of PPV, which the authors claimed is 1000 times more sensitive than RT-PCR.
Direct real-time PCR (drtPCR) was used by Kim et al. (2008) to detect PPV in samples from large-scale field tests.
Prevention and ControlTop of page
There is no anti-virus treatment available to control sharka disease in orchards. However, there are considerable differences in susceptibility between the cultivars available for use in countries where infection is widespread (Hamdorf, 1986; Kegler et al., 1989; Mainou and Syrgianidis, 1992). Biological control by inoculation of trees with hypo-aggressive strains has not been as successful in the field as under controlled conditions (Kerlan et al., 1980).
Other effective control methods are to produce healthy plants for planting within a certification system, to control aphid vectors by regular treatment with aphicides, and to destroy diseased trees in orchards. Such methods are being used to contain PPV in several countries (for example, France and Italy) (Barba, 1998; Kegler and Hartmann, 1998).
EPPO recommends a certification scheme for fruit trees, which takes account of PPV (OEPP/EPPO, 1991/1992). Resistance to PPV has been reviewed by Dosba et al. (1994) and Kegler and Hartmann (1998) and this approach shows some promise, whether by traditional breeding or selection by transgenic methods (Câmara Machado et al., 1992b; Escalettes et al., 1994; Ravelonandro et al., 1998b; Scorza et al., 1998). New PPV-resistant plum, apricot, peach, and nectarine cultivars were bred or selected with different types or mechanisms of PPV-resistance (Hartmann, 1998; Kegler and Hartmann, 1998; Lahmatova et al., 1998; Paprtsein et al., 1998; Polák, 1998; Rankovi and Paunovi , 1989; Toma et al., 1998; Scorza et al., 2007). Studies of resistance to PPV in apricots showed that resistance appeared to be under simple genetic control involving one gene locus (Karayiannis, 2006).
EPPO recommends that all imported host material (except seeds) should come from a field subject to growing-season inspection. If the virus is present in the exporting country, this inspection should also concern the immediate vicinity of the field, and the material should derive from tested mother plants (OEPP/EPPO, 1990).
ReferencesTop of page
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ContributorsTop of page
26/02/2008 Updated by:
Vern Damsteegt, USDA-ARS, Foreign Disease-Weed Science Res Unit, Ft. Detrick, MD 21702, USA
Distribution MapsTop of page
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