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| 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.
