Details of DPV and References

DPV NO: 410 November 2005

Family: Potyviridae
Genus: Potyvirus
Species: Plum pox virus | Acronym: PPV

This is a revised version of DPV 70

Plum pox virus

Miroslav Glasa Institute of Virology, Department of Plant Virology, Slovak Academy of Sciences, Dúbravská cesta 9, 84505 Bratislava, Slovakia

Thierry Candresse UMR GDPP, INRA and University of Bordeaux 2, IBVM, Centre INRA de Bordeaux, BP 81, 33883 Villenave d'Ornon Cedex, France



Observed around 1915 on plum in Bulgaria, the disease was first described by Atanasoff (1932). It was reported on apricot in 1933 (Atanasoff, 1935), on peach in 1961 (Németh, 1963) and on sour cherry in the 1980's (Kalashyan et al., 1994).

Selected synonyms
Prunus virus 7, Annulus pruni, Sharka virus, Prunus broad streak and ringspot variegation virus (Németh, 1986)

PPV is an RNA virus with flexuous filamentous particles approximately 750 x 15 nm. It has a wide geographical distribution (Europe, North Africa, Asia, Americas) and a natural host range restricted to Prunus spp. It is transmitted by several aphid species in a non-persistent manner, is graft-transmissible to susceptible Prunus spp. and sap-transmissible to a wide range of herbaceous species, but is not seed-borne. PPV causes economic losses in cultivated stone fruit species (plum, apricot, peach).

Main Diseases

Causes the Sharka or "plum pox" disease of Prunus spp. - plum, apricot, peach, sour cherry and sweet cherry. Symptoms vary depending on host susceptibility, virus isolate and environmental conditions but generally affect both leaves and fruits. Mixed infection with other viruses such as Prunus necrotic ringspot virus or Prune dwarf virus may increase the severity of symptoms.

Geographical Distribution

Europe, Mediterranean Basin, Asia Minor, China, South (Chile, Argentina) and North (USA, Canada) America. Not reported from Australia or New Zealand. Unconfirmed report from India.

Host Range and Symptomatology

Natural host range covers species of the genus Prunus including cultivated stone fruits - plum (P. domestica), Japanese plum (P. salicina), apricot (P. armeniaca), peach and nectarine (P. persica), sweet cherry (P. avium) and sour cherry (P. cerasus). Wild and ornamental trees, such as myrobalan (P. cerasifera), American plum (P. americana), dwarf flowering almond (P. glandulosa) and blackthorn (P. spinosa) act as local reservoirs of the virus (Polák, 1997; Labonne et al., 2004).

Experimental host range is large, with over 60 reported host species in eight families (Van Oosten, 1970, 1971).

Symptoms in plum consist generally of chlorotic spots or rings, oak-leaf patterns and vein clearing on leaves (Fig. 1), and shallow ring or arabesque depressions on fruits, sometimes with brown or reddish necrotic flesh and gumming (Fig. 2). Fruits may drop prematurely. Tolerant plum cultivars (i.e. Cacak Best, Stanley) show no symptoms on fruits.

Infected apricots develop chlorotic or pale-green rings and lines on leaves (Fig. 3), and light coloured depressed rings on fruits (Fig. 4), which may be severely deformed and fall prematurely in the most susceptible varieties. Typical discoloured rings occur on stones (Fig. 5).

Symptoms in peach are often less conspicuous. Vein clearing, small chlorotic blotches and distortion of the leaves (Fig. 6) develop in susceptible genotypes. Flower breaking is observed in some varieties. Pale rings or diffuse bands are visible on the skin of the fruits (Fig. 7), which may fall prematurely.

In almond, infection is often symptomless.

In cherry, pale green patterns and rings appear on leaves, and fruits are slightly deformed, with chlorotic and necrotic rings, notched marks and premature fruit drop (Fig. 8).

Diagnostic species
Woody indicators:

Prunus persica cv. GF305 - vein clearing and distortion of the leaves (Bernhard et al., 1969) (Fig. 9).

P. tomentosa - chlorotic mottle, vein chlorosis, leaf deformation, necrotic spots (Damsteegt et al., 1997).

Prunus marianna cv. GF8.1 - diffuse chlorotic spots on leaves.

Prunus insititia cv. St. Julien no.2 - chlorotic spots and rings (Fig. 10).

Prunus domestica K4 (Kirke × Persikovaja), hypersensitive hybrid - pale green leaf mottling, necrotic leaf spots, shoot tip necrosis and/or eventual decline, depending on the isolate (Kegler et al., 2001).

Herbaceous indicators:

Chenopodium foetidum - chlorotic, chloro-necrotic or necrotic spots depending on the viral isolate (Fig. 11). Infection is not systemic.

Nicotiana benthamiana - stunting, chlorotic mosaic with dark green islands, leaf puckering (Fig. 12).

N. clevelandii or N. clevelandii × N. glutinosa hybrid - chlorotic or necrotic local lesions, systemic chlorotic mottling. Some isolates induce very mild or no symptoms.

Pisum sativum (cv. Colmo, Express Généreux, Serpette d´Auvergne) - light green mosaic, chlorotic mottling.

Non-host species

Species described as non-hosts include Crataegus monogyna, Cucumis sativus, Cucurbita pepo, Datura stramonium, Malus domestica, M. sylvestris, Prunus serrulata, Pyrus communis, Solanum nodiflorum and S. rostratum.

Propagation species

Pisum sativum, Nicotiana benthamiana, N. clevelandii, N. clevelandii × N. glutinosa or N. occidentalis are suitable sources of virus for purification, 14-21 days after inoculation.

Assay species

Chenopodium foetidum is a useful local lesion host.


Initially, different strains were described on the basis of symptoms in various experimental hosts. According to the symptoms on Chenopodium foetidum, Sutic et al. (1971) classified PPV isolates as yellow, intermediate and necrotic strains. However, no relationships could be established between biological and serological/molecular properties.

On the basis of molecular and serological properties, six strains/subgroups have been recognized (Kerlan & Dunez, 1979; Wetzel et al., 1991; Bousalem et al., 1994; Nemchinov et al., 1996; Candresse et al., 1998; James et al., 2003; Glasa et al., 2004).

PPV-M (Marcus). First identified in peach in Greece. Present in many European countries but absent from the Americas. Causes rapidly spreading epidemics in peach (Dallot et al., 1998) but is less frequently found in plums. PPV-M isolates are usually efficiently transmitted by aphids.

PPV-D (Dideron). First isolated from apricots in southeastern France. PPV-D isolates are present in all areas where PPV has been reported. Infrequently found in peach. PPV-D isolates are often described as causing slower spreading epidemics and being less efficiently transmitted by aphids than PPV-M but this cannot be generalized.

PPV-Rec (recombinant). Recognized only recently through the use of improved strain-typing methods. A group of isolates derived from a single homologous recombination event between PPV-M and PPV-D (cross-over in the 3' terminal part of the NIb gene). Widespread in several central and eastern European countries. Frequently associated with plums, and efficiently transmitted by aphids.

PPV-EA (El Amar). Originally isolated from apricots in Egypt, and not reported outside this country thus far.

PPV-C (Cherry). First reported from Moldova in sour cherry in the 1980's. Reported in (and subsequently eradicated from) sweet cherry in Italy. Sporadically present in central and eastern European countries. PPV-C isolates are the only ones to infect cherry systemically. Able to infect other Prunus species under experimental conditions (Bodin et al., 2003).

PPV-W (Winona). Reported (and eradicated) from two infected plum trees in Canada.

Transmission by Vectors

Transmitted in a non-persistent manner, but with wide variations in efficiency, by over twenty different aphid species, including Aphis craccivora, A. gossypii, A. hederae, A. spiraecola, Brachycaudus cardui, B. helichrysi, B. persicae, Myzus persicae, M. varians, Phorodon humuli and Rhopalosiphum padi (Kunze & Krczal, 1971; Labonne et al., 1995). The DAG amino acid motif, located near the N-terminus of the capsid protein, is highly conserved in aphid-transmissible PPV isolates and loss of transmissibility is correlated with deletion of this motif (Maiss et al., 1988).

Transmission through Seed

Conflicting results have been reported in the past concerning seed transmission in some Prunus species. Recent studies have failed to demonstrate seed transmission of PPV in any of its woody hosts (Myrta et al., 1998b; Glasa et al., 1999).

Transmission by Dodder

No reports.


The virus is a relatively good immunogen and high quality antisera have been obtained and used in serological detection techniques (ELISA, ISEM, immunoblot, immunocapture RT-PCR). Monoclonal antibodies have been produced and their reactivity analyzed, allowing the identification of at least one broad-reactivity monoclonal antibody (Cambra et al., 1994; Candresse et al., 1998). Strain-specific monoclonal antibodies have also been obtained for isolates belonging to the PPV-M (Boscia et al., 1997), PPV-D (Cambra et al., 1994), PPV-EA (Myrta et al., 1998a) and PPV-C (Myrta et al., 2000) strains, but a few rare isolates may be wrongly typed using these reagents (Candresse et al., 1998).


The comparison of complete genomic sequences revealed 10.6-26.6% nucleotide divergence among representative isolates of the PPV-M, D, Rec, C and W strains (Fanigliulo et al., 2003; Glasa et al., 2004; James & Varga, 2005). Comparisons using partial sequences indicate that PPV-EA probably falls within the same divergence interval.

Recombination has played a significant role in the evolutionary history of PPV. PPV-C (and probably PPV-EA and PPV-W) appear to constitute independent evolutionary lineages. PPV-D and PPV-M share an ancestrally recombined 5' part of their genome (5' non-coding region, P1, HC-Pro and N-terminus of the P3) (Glasa et al., 2004). In addition, a divergent PPV-M isolate from Turkey (Ab-Tk) derives from a different recombination event affecting the same region, with a breakpoint in the HC-Pro gene (Glasa & Candresse, 2005). PPV-Rec derives from a recombination between PPV-D and PPV-M with a breakpoint in the C-terminus of the NIb gene (Glasa et al., 2004).

Assays that allow discrimination between the various PPV strains include serological analysis with strain specific monoclonal antibodies (Candresse et al., 1998), RFLP analysis of PCR fragments derived from the coat protein (Bousalem et al., 1994; Candresse et al., 1998), P3-6K1 (Glasa et al., 2002a) and CI regions (Glasa et al., 2002b), or PCR with strain specific primers (Candresse et al., 1998) and sequence analysis. With a few rare isolates, both monoclonals and RFLP techniques have been shown to provide erroneous results (Candresse et al., 1998). In addition, proper identification of recombinant isolates may require the use of several techniques targeting different parts of the viral genome or specific primers with binding sites located on either side of the recombination crossover.

Stability in Sap

The in vitro biophysical properties are variable according to the isolate and the plant species used for propagation. The thermal inactivation point (10 min) is about 51-54°C in Nicotiana clevelandii sap (Cropley, 1968), and 45-47°C in Chenopodium foetidum sap (Kegler et al., 1964). Dilution end-points in sap from these two hosts are 10-4 and 10-1, respectively. Infectivity is retained at 20°C for 1-2 days.

Long term conservation of virus cultures can be achieved by freeze-drying or by desiccation of leaf material over anhydrous calcium chloride.


1. Schade (1969). Homogenize 100 g systemically infected Nicotiana clevelandii leaf tissue in 300 ml distilled water containing 0.3% (w/v) ascorbic acid and 0.01 M sodium diethyl dithiocarbamate (DIECA). Shake for 5 min with an equal volume of cooled chloroform. Centrifuge for 15 min at 1000 g and 15 min at 5000 g, retaining the aqueous phase at each step. Concentrate the virus by one cycle of high and low speed centrifugation, resuspending the virus in 0.05 M borate buffer, pH 8.2. Normal plant proteins may be removed by absorption with host-specific antisera.

2. Lain et al. (1988). Harvest systemically infected leaves of N. clevelandii or N. benthamiana 20-30 days after inoculation. Homogenize leaf tissues with 0.5 ml/g of a mixture of 3 parts 0.18 M McIlvain's citric acid - phosphate buffer pH 7, containing 0.2% thioglycolic acid, 0.01M DIECA-Na and 0.5M urea, and 1 part chloroform. Centrifuge the homogenate for 10 min at 6000 g and then centrifuge the supernatant for 1.5 h at 57500 g. Resuspend the pellet in 1/2 vol. of 0.01M citric acid-phosphate buffer containing 0.2% 2-mercaptoethanol and 1M urea. Proceed then through one cycle of differential centrifugation (high speed concentration, low speed clarification, high speed concentration). Resuspend the final pellet in 0.02 vol. of borate-EDTA buffer and centrifuge in 10-40% sucrose gradients at 75000 g for 1.5 h. The purified virus is resuspended in 50mM sodium borate buffer pH 8.2. Virus yield is about 1-4 mg per 100 g of fresh leaves.

Other suitable purification methods include: Rankovic & Jordovic (1970), Van Oosten (1972) and Albrechtová et al. (1986).

Properties of Particles

Sedimentation coefficient: 180 S.

A260/A280 ratio: 0.77-0.87.

Particle Structure

PPV has typical potyvirus particles. Particles are flexuous filaments without envelopes, reported to be about 760 nm long and 20 nm wide (Kegler et al., 1964) or 725-750 nm long (Babovic et al., 1971).

Particle Composition

The particles are exclusively made of a single-stranded genomic RNA encapsidated in a single type of capsid protein subunit. The RNA comprises 9741-9795 nucleotides, with a polyadenylated 3' end and a virus-encoded protein (VPg) covalently bound to the 5' end. The molecular weight of the capsid protein subunit has been estimated electrophoretically to be 36-38 kDa (Dallot et al., 1998) and calculated from the nucleotide sequence to be 36.3-36.7 kDa.

Genome Properties

Full-length sequences are available for 14 PPV isolates, including 8 of PPV-D [Dideron (X16415), NAT (D13751, NC_001445), SC (X81083), PENN-1 (AF401295), PENN-2 (AF401296), Fantasia (AY912056), Vulcan (AY912057) and 48-922 (AY912058)], 2 of PPV-M [PS (AJ243957) and SK68 (M92280)], 1 of PPV-Rec [BOR-3 (AY028309)], 2 of PPV-C [Soc (Y09851) and SwC (AY184478)] and PPV-Winona (AY912055). Partial sequences are available for a wide range of isolates, including PPV-El Amar (X56258). The genomic organisation is typical of potyviruses. The genome encodes a single large polyprotein precursor (3125-3143 aminoacids, about 355 kDa), which is proteolytically processed by three virus-encoded proteinases (P1-Pro, HC-Pro and NIa-Pro) to yield as many as 10 functional proteins (Fig. 13). The capsid protein domain maps to the carboxy-terminus of the polyprotein (López-Moya et al., 2000).

Relations with Cells and Tissues

Needle-shaped inclusions and X-bodies are abundant in the nucleus and in the cytoplasm of cells of systemically infected herbaceous hosts such as Nicotiana clevelandii (Plese et al., 1969; Van Oosten & Bakel, 1970) and in the leaves and ripe fruits of infected plum and peach trees. 'Pin-wheel' inclusions occur in leaf cells of plum, peach and Chenopodium foetidum (Bovey, 1971).

In woody hosts, the virus is unevenly distributed and full systemic invasion of a tree may require several years (Bodin-Ferri et al., 2002). Long distance viral movement is restricted in some resistant (apricot, peach) and hypersensitive (plum) genotypes. Similarly, most PPV isolates (except PPV-C) remain restricted close to the inoculation point in cherry and in Prunus mahaleb.

Ecology and Control

Natural spread occurs through aphids from neighboring infected reservoirs (cultivated, wild or ornamental trees). No epidemiologically significant contribution of weeds or annual herbaceous plants to the spread of Plum pox virus has been reported. Long range introduction of the virus is linked to international exchange of contaminated propagation material. The main strategies to control the disease are either (a) quarantine measures for unaffected areas or (b) a mix of prophylactic approaches in regions where the disease is present but under control. The latter include the use of virus-free propagation material (rootstock, budwood), the eradication of infected plants and, if required, the control of aphid populations. Such a mixed strategy has been shown to slow virus progress but complete eradication is notoriously difficult to achieve. Attempts at using cross-protection with attenuated virus isolates have not met with success in the case of PPV (Kerlan et al., 1980).

Wide differences exist in the susceptibility to PPV of individual varieties. In regions where the spread of the disease is no longer under control (central and southeastern Europe), the cultivation of less susceptible or tolerant varieties may allow the continuation of production. This practice, however, further contributes to viral spread.

Resistant plum and apricot genotypes have been identified. In peach, no resistant varieties are known but resistance has been identified in the wild relative Prunus davidiana (Kegler et al., 1998). Breeding efforts are ongoing in these various species to introduce the resistance from the identified sources into commercially acceptable varieties. Progress is, however, slowed by the long generation times, the length of the resistance tests and the generally polygenic nature of the resistance involved. Breeding of plum genotypes with a hypersensitive response to PPV infection may be another promising way to produce resistant plum varieties (Hartmann, 1998).

Genetically modified plum clones carrying the PPV capsid protein gene have shown high resistance to PPV infection (Scorza et al., 1994). Although the resistance can be overcome by graft-inoculation, it seems to provide effective protection against the natural spread of PPV in several field tests, even under conditions of high natural inoculation pressure (Malinowski et al., 1998).


To date, PPV is the only potyvirus reported to infect Prunus crops. Serological cross-reaction with PPV has occasionally been reported from PPV-free Prunus samples (James et al., 1994; Hari et al., 1995; James et al., 1996) originating, in particular, from Asia. Partial characterization of the cross-reacting agent(s), tentatively named "Asian Prunus latent virus" or "Plum-pox like virus", has so far mostly yielded confusing results, in part because the various plant sources appear to harbour complex mixed infections. The agent responsible is, however, most likely not a potyvirus but, given the quarantine status of PPV, has clear quarantine implications.


References list for DPV: Plum pox virus (410)

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