Mechanism Of Cross-protection Research Articles

Control of plant pathogens with viruses and related agents

Cytoplasmically transmissible agents causing diseases of plant pathogenic fungi characterized by reductions in pathogenicity, ability to form sexual and asexual spores, spore viability and growth rate, are often associated with the presence of one or more specific segments of virus-like double-stranded RNA (dsRNA). In Italy, hypovirulent dsRNA-containing strains of the chestnut blight fungus,Endothia(Cryphonectria)parasitica, have become predominant in many areas where blight is no longer a serious problem. dsRNA-containing strains of other pathogens, with various degrees of debilitation, survive in natural populations but have not become predominant or resulted in any great reduction in disease. Examples include the Dutch elm disease fungus,Ophiostoma(Ceratocystis)ulmi, and the wheat take-all fungus,Gaeumannomyces graminisvar.tritici. Successful biological control of such pathogens could probably be achieved, however, if methods could be developed to suppress the loss of dsRNA that occurs during the sexual and other stages of their life cycles, and to suppress the vegetative incompatibility reactions that reduce the cytoplasmic transmission of dsRNA. Systemic infection with attenuated strains of plant viruses can protect plants from later infection by virulent strains of the same or closely related viruses. Despite some notable successes, e.g. control of citrus tristeza and tomato mosaic viruses, such ‘cross-protection’ has not been widely applied because of the cost and difficulty of application, and caution about the widespread distribution of infectious agents in the environment. These problems could be overcome if cross-protection could be achieved by the expression of a single viral gene rather than infection with intact virus, and consideration of possible mechanisms of cross protection suggests novel ways of producing virus-resistant plants.

A proteinless mutant of tobacco mosaic virus: evidence against the role of a viral coat protein for interference.

A coat-protein-free mutant of tobacco mosaic virus as well as mutants with a non-functional coat protein were found to interfere with the establishment and spread of challenging strains of TMV. The results do not support an earlier concept, according to which the genome of a related challenging virus could be captured by the coat protein of the virus introduced in advance. The presence of a viral coat protein is obviously not essential and a competition among the viral genomes for some specific site seems to be a more likely mechanism of cross protection.

Beziehungen Zwischen Den Pilzen Gaeumannomyces Graminis Und Phialophora Radicicola Bei Gemeinsamem Wachstum AußErhalb Der Wirtspflanze

In laboratory model experiments, numerous hyphal adhesions were found to take place between a severe wheat pathogen, G. graminis var. tritici, and a weak wheat pathogen, P. radicicola var, radicicola, and therefore the linear growth of the both fungi is inhibited. When both fungi occur concurrently side by side on celophane, the hyphae of one fungus do not occupy the place colonized before by the other fungus, due to mutual contact. It can be presumed that also direct interaction between hyphae of both fungi participates in cross protection mechanism of the take-all fungus G. graminis with P. radicicola.

Studies on the Mechanism of Viral Cross Protection

Studies on the Mechanism of Viral Cross Protection

Studies on the mechanism of cross-protection in cereal rusts

Using a spore settling tower to inoculate oat leaves uniformly with known densities of urediniospores of oat and wheat rusts, a quantitative study was made to investigate the mechanism of cross-protection in cereal rusts. The number of pustules produced per unit area of leaf surface by oat rusts was markedly reduced by prior inoculation with viable urediniospores of either wheat or oat rusts. Non-viable spores failed to induce cross-protection. The degree of cross-protection varied directly with the inoculum density of the preinoculated rust. Maximal cross-protection occurred when the interval between successive inoculations was 4 days or more. Microscopic examination of the infection process showed that if an oat rust produced appressoria over stomata which were already occupied by appressoria of the preinoculated rust, penetration failed to occur and the infection process was stopped. If, however, appressoria were produced over stomata not already occupied by appressoria of the previously inoculated rust, the frequency of penetration was the same as that on uninoculated control leaves. It would seem that the halting of the infection process at the penetration phase was responsible for cross-protection in cereal rusts.

Cross-protection against the wheat and oat take-all fungi by Gaeumannomyces graminis var. graminis

Glasshouse experiments have shown that the prior colonisation of wheat roots by Gaeumannomyces graminis var. graminis, a fungus closely related to the wheat and oat take-all fungi but non-pathogenic to temperate cereals, reduced take-all infection along the roots. Cross-protected wheat plants produced grain yields significantly greater than those of unprotected plants but not significantly different to those of healthy wheat plants. A Phialophora-like fungus from grass roots did not confer the same degree of protection. There is some evidence that the cross-protection mechanism may be a specific host response nduced by var. graminis. The possible use of var. graminis in the biological control of take-all is discussed.

Studies on cross-protection in the anthracnose disease of bean

Leaf, pod and hypocotyl tissue of Phaseolus vulgaris inoculated with incompatible races of Colletotrichum lindemuthianum was protected against anthracnose caused by compatible races of this organism. Protection of excised hypocotyls was localized within areas receiving spores of the incompatible race and was seen as an effect of the host on the growth of established intracellular hyphae of the compatible race rather than on spore germination or penetration. Host cells close to those showing browning in response to an incompatible race seemed abnormally sensitive to the presence of hyphae of the compatible race and underwent earlier necrosis than comparable cells in unprotected tissue. They also showed a greater sensitivity to mild heat treatments. Culture filtrates of both compatible and incompatible races caused protection of exposed hypocotyl cortex tissue apparently by inducing the formation of germination inhibitors by the host. The active components of these filtrates were water soluble and heat stable. The possible mechanisms of cross-protection are discussed in view of this research and the work of others.

The mechanism of cross-protection afforded by dengue virus against West Nile virus in hamsters.

The protection afforded by similar concentrations of different dengue virus serotypes against a subsequent challenge of West Nile virus was studied in hamsters. The New Guinea C strain of dengue 2 virus gave the best protection. It was found that the anamnestic neutralizing antibody response induced by the challenge West Nile virus against West Nile virus in hamsters, previously immunized with dengue 2 virus, might play a major role in the cross-protection observed in this system.