Resistance
to disease of plants has historically been divided into two major categories:
non-host resistance and host resistance. The former, which encompasses the case
where all genotypes within a plant species show resistance or fail to be
infected by a particular virus, specifically signifies the state where genetic
polymorphism for susceptibility to a particular virus has not been identified
in a host taxon. Clearly, most plant species are resistant to most plant
viruses. Susceptibility is the exception to the more general condition of
resistance or failure to infect.
Although
underlying mechanisms of non-host resistance to viruses are largely unknown and
are likely as diverse for viruses as they are for other classes of plant
pathogens, improved understanding of the ways in which infection fails in these
interactions may be particularly important for breakthroughs in the development
of plants with durable broad-spectrum disease resistance. Host resistance to
plant viruses has been more thoroughly investigated, at least in part because,
unlike non-host resistance, it is genetically accessible. This general case,
termed host resistance, specific resistance, genotypic resistance, or cultivar
resistance, occurs when genetic polymorphism for susceptibility is observed in
the plant taxon, i.e., some genotypes show heritable resistance to a particular
virus whereas other genotypes in the same gene pool are susceptible.
In
resistant individuals, the virus may or may not multiply to some extent, but
spread of the pathogen through the plant is demonstrably restricted relative to
susceptible hosts, and disease symptoms generally are highly localized or are
not evident. The distinction between resistance to the pathogen and resistance
to the disease is important to articulate. Resistance to the pathogen typically
leads to resistance to the disease; however, resistant responses involving
necrosis can sometimes be very dramatic, even lethal, e.g., the N gene
in tobacco for resistance to Tobacco mosaic virus (TMV) or the I gene
in Phaseolus vulgaris for resistance to Bean common mosaic virus.
In the case of resistance to disease symptoms or tolerance to the disease, the
virus may move through the host in a manner that is indistinguishable from that
in susceptible hosts, but disease symptoms are not observed. If the response is
heritable, these plants are said to be tolerant to the disease, although they
may be fully susceptible to the pathogen. This host response is very prevalent
in nature, and has been used to considerable benefit in some crops, e.g., the
control of Cucumber mosaic virus (CMV) in cucumber, even though the
genetic control of this response is typically difficult to study. The genetics
of tolerant responses are not be considered further due to the complexity of
the biology and relative lack of information. More recently, a third important
category of host resistance has been identified, initially in studies involving
TMV: systemic acquired resistance (SAR).
This
response can be activated in many plant species by diverse pathogens that cause
necrotic cell death, resulting in diminished susceptibility to later pathogen
attack. As SAR has recently been reviewed, this topic is not discussed further
here. Virus-induced gene silencing, another induced defense mechanism to virus
disease, has also been reviewed recently. Transgenic approaches to plant virus resistance
have been widely explored since the earliest experiments where by transgenic
tobacco plants expressing TMV coat protein (CP) were challenged with TMV and
shown to be resistant. It is now possible to engineer resistance and tolerance
to plant viruses using transgenes derived from a wide range of organisms
including plant-derived natural R genes, pathogen-derived transgenes, and even
non-plant and non-pathogen-derived transgenes.
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