Thursday, March 14, 2013

A crash course on virus disease control

Photo: G Fernandez, 2012.

The following article was provided courtesy of the authors. They wrote it in response to a need to educate growers and others about some of the basic science that is behind virus infection and control of viruses in plants. 

A crash course on virus disease control

Ioannis E. Tzanetakis, Dept. of Plant Pathology, Division of Agriculture, University of Arkansas System
Robert R. Martin, USDA-ARS, Horticultural Crops Research Laboratory, Corvallis, OR

Not all people are aware that plants can be infected by viruses. Still, plant viruses account for losses in the billions of dollars every year. There have been several cases where a virus epidemic has disseminated crops in vast areas and the most frustrating part from a grower’s standpoint is that there is not much to do once a plant is infected.

Let’s start from the basics: What is a virus? A virus is an obligate parasite consisting of nucleic acids (RNA or DNA), proteins and in some cases, lipid membranes. The key term here is ‘obligate’. Viruses cannot function outside a living cell. If the host dies, the virus goes with it. Thus, in nature viruses have co-evolved with their hosts to keep a fine balance between virus replication and survival, and survival of the host to sustain infection through dormant seasons of the host. This is definitely the case in the majority of plant-virus interactions. Viruses have evolved to co-exist and most have minimal impact on their hosts. With new technologies developed in the last few years we know for a fact that plants are infected with several viruses but in most cases no definite symptoms are observed. These are what we refer to as ‘resident’ or ‘latent’ viruses.

But there are also cases where viruses cause severe plant disease and even death. This is truly an imbalance in the system. The majority of the scientific community agrees that viruses that kill their hosts are probably accidental introductions, as they die out along with their hosts. There are rare cases where viruses can mutate to cause less severe symptoms allowing for their survival in a particular host.

As we learn more about viruses and virus diseases we have come to realize that, at least in berry crops, the majority of disease are not caused by a single virus but rather by the combination of two or more viruses. In the past, scientists were able to identify the ‘easy’ viruses, entities that were easy to isolate and manipulate. With the new technologies that have been developed, we now realize that the knowledge of the past only accounts for the tip of the iceberg in terms of what causes virus diseases in berry crops. A clear example is blackberry yellow vein disease (BYVD). Until the turn of the century people assumed that symptoms were caused by Tobacco ringspot virus (TRSV). Although TRSV is found in some plants, the majority of symptomatic plants are free of the virus.  Also, TRSV does not cause symptoms in single infections in most modern blackberry cultivars. We now know that BYVD is caused by complexes, with more than a dozen viruses that may contribute to the symptoms.  BYVD can be caused by various combinations of these viruses, and in all cases observed to date, there are at least two and up to seven viruses involved.
Management strategies of virus diseases are based on resistance, control of vectors or elimination of viruses from propagation material.  Resistance is based on the premise that viruses are identified by their hosts as invaders at the genetic level that results in some step in the virus life cycle being blocked. Given that most virus disease in berry crops are caused by complexes it is a challenging undertaking to develop multiple virus resistances. If symptoms are expresses in the presence of multiple viruses then plants need to be able to recognize all or most of those entities. If a single pathogen causes disease it is easy to screen and identify resistant sources. However, in berry crops, resistance sources have not been identified for most of the viruses. Resistance to multiple viruses is more challenging as different combinations need to be introduced to plants and the reaction to each virus needs to be evaluated. When breeders work with thousands of accession, the challenge is obvious.

Vector control can be a good alternative but knowledge of the epidemiology and transmission of viruses is necessary for the implementation of a successful control program. There are four different modes of transmission when it comes to viruses and their vectors: a. non-persistent; b. semi-persistent; c. circulative and d. circulative propagative. What do those terms mean? In the non-persistent transmission, virus acquisition and transmission takes place in few seconds or minutes and the vector losses the ability to transmit in minutes. In the case of semi-persistent viruses the vector needs to feed on the source plant for several minutes or even hours, but once the virus is acquired it may be able to transmit from hours to days. The latter two modes of transmission are more complicated as vectors need hours or even days of feeding on infected material to acquire the virus. Then, they are unable to transmit for hours or even days as the virus need to pass though vector membranes to make it back into the salivary system.  However, once acquired, they are able to transmit for days, weeks or even the life of the vector. In the case of circulative propagative viruses, the virus actually infects the vector and in certain cases, it has been proven that they can move to the next generation though infection of the egg.

But why is this important to know? The secret to an effective control regime lies in the knowledge of how viruses are vectored. In the cases of the circulative viruses the answer is straight forward, since there are days between when a vector acquires a virus before it can transmit, allowing for ample time to control the vector. Control will probably eliminate the vector before it is able to move viruses to adjacent plants. How about the case of non- and semi-persistent transmission? This presents a major challenge: Let’s assume the case of a non-persistent virus. The vector transmits the virus after short feeding time. A control agent applied to the foliage may change the vector behavior (e.g. the composition of the plant sap has changed) such that the vector does not settle down, but rather moves from plant to plant, thus increasing the number of plants that it infects.  If no control was applied only a single plant would be infected. This situation is very specific and changes depending the environment, the control agent/chemical and of course the virus/vector combination. Without this information the grower may use valuable resources for vector control and that leads to increased virus spread.

Breeding for vector resistance can be effective at controlling all viruses transmitted by the vector.  Probably the best example of this in all of plant virology, is the success of aphid resistance in virtually eliminating the spread of the raspberry mosaic complex, a group of three aphid-transmitted viruses.  Even though successful in North America for more that 50 years, the original source of aphid resistance has been overcome by new biotypes of the aphid and this resistance is no longer effective.  In Europe, the resistance was overcome much more quickly and now multiple aphid resistance genes have been overcome.  It must be remembered that if we look at a complex like BYVD, there are multiple types of vectors involved (eriophyid mites, whiteflies, nematodes, thrips and pollen, which makes breeding for vector resistance a monumental task.  Also, in most cases, vector resistance has not been identified in the berry crops

The easiest and most effective control is planting clean material. Many growers propagate their own stock for planting new fields. Whereas this appears to be an easy and cost-effective approach it can have devastating results. Plants may appear normal but this is not uncommon when infected with one or two viruses. When placed in the field, viruses are transmitted between plants and complexes develop, plus additional viruses may be vectored into the field and a field decline may become apparent shortly after planting. Even if there are no apparent symptoms, virus infection may account to a 5-20% yield loss. Establishing a field with virus-tested plants does not mean that they will never get infected. As a law of nature, all organisms from bacteria to amoebas to plants and primates get infected by viruses. A field with clean plants will stay productive for more time and yield better than a field with infected plants, providing growers with better quality product and better yields.
There have been several cases where growers move self-propagated plants to new areas and introduce new pests to new environments. The introduction of a few Prunus trees infected with Plum pox virus has cost the tax payers hundreds of millions of dollars. Citrus greening is another example of how the inappropriate movement of plant material can cause losses of colossal proportions. So when growers plant their next field they need to recognize the extra investment of virus-tested plants not only in terms of profitability of the newly planted field. But, also in terms of protecting existing fields on the same farm or in the area from the introduction of new viruses that could jeopardize production. It is certain that the return of this investment will be greater that the risk of disseminating viruses. 

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