Plum Pox Virus
Original observations of Plum pox virus (PPV) were made by plum growers in Bulgaria in the mid 1910s. PPV was detected in October 1999 in Adams County, Pennsylvania. During 2000, separate infestations of plum pox virus were detected in Ontario and Nova Scotia, Canada. In 2006, PPV was confirmed in New York and Michigan. The virus commonly is known in Europe as Sharka. Levy et al. (2000) reports the following status and geographic distribution of the plum pox virus:
- Restricted Distribution – Albania, Austria, Cyprus, Czech Republic, France, Italy, Luxemburg, Moldova, Norway, Portugal, Southern Russia, Slovenia, Spain, Syria, Turkey, Ukraine, United Kingdom, United States
- Widespread – Bulgaria, Croatia, Germany, Greece, Hungary, Poland, Romania, Slovakia, Former Yugoslavia
- Introduced, Established – Azores, Bosnia-Herzegovina, Egypt, Former USSR, India, Lithuania
- Introduced, Presumably Eradicated – Belgium, Netherlands, Switzerland
- Present Status Unknown – Chile, Denmark
It is important to note that in general, the virus is widespread in some countries and of limited distribution in others.
The virus does not kill trees but causes yield losses and reduces the marketability of fruit. For example, PPV has caused considerable losses in Europe, with susceptible cultivars reporting yield losses of 80-100% (Levy et al. 2000).
Plum pox virus belongs to the genus Potyvirus in the family Potyviridae and has virions which are flexuous filaments with no envelopes (Levy et al. 2000). The plum pox virus has been characterized into 4 different serological strains based on biology, serological reactions, and molecular and biological data: M, D, EA, and C (Levy et al. 2000). PPV-D is the most common strain in Western Europe and is the only strain currently found in the US and Canada (Levy et al. 2000). PPV-M is considered to be a more aggressive, epidemic form and is the most common strain in Southern, Eastern, and Central Europe. Peach is most susceptible to PPV-M. PPV-EA has only been isolated in the North Africa region. PPV-C is present in Eastern and Central Europe, and sweet and tart cherries are most susceptible to this strain.
PPV symptoms may appear on leaves, fruits, flowers, and seeds and may show an uneven distribution within the tree. In some cases, symptoms may not occur even though an infection is present. Infections are not actually transmitted through the fruit. The severity of symptoms depends upon the plant species and cultivar, PPV strain, season, temperature, and location (Levy et al. 2000). Leaves and fruit may show yellowing and browning ring patterns, bands, or blotches. Apricot and plum fruit can be misshapen and deformed with rings present on their stones. Flowers may have streaking on the petals or pigmented ring patterns. Also, symptoms can be absent or only present during the growing season. Varied host susceptibility may also occur depending upon the PPV strain.
The natural hosts of PPV are restricted to the genus Prunus, infecting peaches, plum, apricots, nectarines, almonds, and sweet and tart cherry (Levy et al. 2000). It also occurs on some ornamental and wild/native Prunus species. The virus has also been artificially introduced to a few other species outside of Prunus as well. Note that not all PPV isolates infect all Prunus hosts. For example, most PPV-D strain isolates do not infect tart cherry.
Introduction of PPV to new regions is usually through propagative materials and distribution of contaminated materials. The virus can be transported in live nursery stock, grafts, and budwood of infected plants. Once in a region, spread can occur rapidly from aphid transmission. Certain factors, such as virus strain, host cultivars, age of the host cultivars, aphid species, and time of year, determine the efficiency of transmission (Levy et al. 2000). For example, the PPV-D strain currently in the U.S. is not vectored as efficiently by aphids as are other strains.
PPV has been transmitted by at least 20 aphid species (transient and colonizing), but only a few are considered important aphid vectors: Brachycaudus cardui, B. helichrysi, Myzus persicae, and Phorodon humuli (Levy et al. 2000). In Pennsylvania, M. persicae and Aphis spiraecola are the most important vectors. The importance of vectors may differ geographically. Aphid transmission occurs over short distances and is know as nonpersistant transmission, which means the virus is infectious and can be transmitted for a short period of time (PDDC 2001). Aphids have a piercing-sucking mouthpart (stylet) that probes into the vascular tissue of plants while feeding. PPV sticks to the food canal and can be injected into another plant as the aphid feeds. The virus can be acquired by probes of 30 seconds and typically transmits within 1 hour of infection (Levy et al. 2000). Most aphids transmit infection no more than 120 meters from the initial source plant (APHIS, USDA). Generally, for aphid virus transmission to be successful it must feed on an infected plant, acquire a sufficient amount of virus, and go immediately to a new host plant for transmission (PDDC 2001). Significant variation in transmission time interval and distance may occur. The virus does not remain or multiply within the aphid once it has been passed on to another plant cell (PDDC 2001). Aphids are responsible for short-distant transmission due to the factors previously explained.
Long distance spread of PPV is caused by physical movement of infected plants or plant parts. Several European introductions have been linked to infected nursery stock or infected buds grafted onto healthy trees (PDDC 2001). Seed transmission has been reported in select cultivars of PPV-M in Eastern and Central Europe, but has not been reported for PPV-D (Levy et. al. 2000). As with aphid transmission, virus strain, host cultivar, and other factors may also affect seed transmission possibilities.
The physical symptoms of PPV may not appear (if at all) on the plant until 3 years after the initial infection but serological tests can detect the virus before symptoms occur (PDDC 2001). Diagnostic hosts, such as Chenopodium foetidum, can be used to detect PPV by mechanical inoculation from suspect hosts (Levy et al. 2000). Woody indicator plants are also useful for detecting the virus by chip budding to hosts. This method allows for the differentiation of the M and D strains based on symptoms. (Levy et al. 2000) Most detection of PPV is conducted through the application of RT-PCR (reverse transcription polymerase chain reaction) technology. Currently, rapid detection of PPV with RT-PCR is achieved with Real-Time PCR. Real-time PCR amplifies target DNA in a similar matter to traditional PCR but cuts down on the number of steps required for detecting PCR products. Most strain typing occurs with monoclonal antibodies or specific primers for RT-PCR. The various strains of PPV may also be differentiated in western blots according to the molecular weight of the viral coat protein, but this method is less commonly used.
It is important to remember that no chemical controls are available to prevent, eliminate, or cure PPV in the field. Once PPV has been detected, it only one infected aphid is necessary to transmit PPV to another tree. Attempts to control aphid populations will not stop the spread of PPV in the field. If you suspect PPV, contact your local cooperative extension agent or NPDN lab for instructions on how to proceed.
The Plant Disease Diagnostic Clinic, Cornell University (2001) lists several management strategies that can be followed to help control the spread of plum pox virus.
- Exclusion and Quarantine – In order to prevent the introduction of the virus into new areas of the US, all plant material should be carefully regulated and inspected. All imported fruit plants should be tested for plant pathogens and growers should purchase only certified virus-free planting stock.
- Eradication – Control spread by eliminating infected trees as quickly as possible. Suspected trees must be sampled multiple times due to the uneven distribution of PPV within a plant. Infected trees should be bulldozed or cut and sucker shoots eradicated with herbicides.
- Insect Control – Attempting to reduce the population of aphids with the application of insecticides. Complete control of aphids is difficult and only one aphid is needed to transmit the virus.
- Plant Breeding and Genetic Engineering – Breeding plant resistance from naturally occurring genes in fruit trees. Genetic engineering may allow scientists to enhance resistance. One breeding success so far has been the transgenic C5 plum. This plum has been bread to contain the PPV coat protein and is highly resistant to PPV. Resistance has been maintained for over 5 years in greenhouse tests using chip bud and aphid inoculation with both the D and M strains of PPV. (Levy et al. 2000)
- Levy, L. Damsteegt, V., Scorza, R., and Kolber, M. 2000. Plum pox – potyvirus disease of stone fruits. The American Phytopathological Society.
- Levy, L. 2001. ELISA laboratory protocols for the plum pox virus national surveillance program. APHIS-USDA.
- APHIS-USDA. Emergency and Domestic Programs – Plum Pox.
- Plant Disease Diagnostic Clinic. 2001. Plum Pox Virus Factsheet. Cornell University.
- A list of federal, state, university, international, and organization websites about Plum Pox Virus can be found at the USDA, National Agricultural Library, National Invasive Species Information Center
We thank Dr. Ruth Welliver, Pennsylvania Department of Agriculture, and Dr. Karen Snover-Clift, Cornell University for their editorial review comments.
These materials may be used as long as the original author is given credit.