If you're a virus using and inevitably damaging your host in order to get yourself replicated you have a few problems to overcome.
First, there is the problem that damaging your host makes it less likely that it'll breed as successfully as non-infected hosts. Secondly, your host's genome will be at an advantage if it develops genes which make it resistant to you. So, you'll inevitably find yourself in a wasteful evolutionary arms race unless you can find a way round these two problems.
Enter the cucumber mosaic virus. This virus infects various members of the cucurbitae group of plants which includes cucumbers, marrows and melons and members of the solanaceae group which includes tomatoes. It is a serious agricultural pest in the latter because it stunts the plants, reduces the yield and spoils the flavour of commercially grown tomatoes.
One way a parasite like a virus can circumvent this tendency to indulge in arms races is to give something back in return; a payback. So the relationship between parasite and host moves closer to being a mutually beneficial, symbiotic relationship. In fact, there are two likely outcomes of a parasite-host relationship: extinction or symbiosis. Obviously the surviving examples are symbiotic illustrating how in the long term selfish genes can produce cooperative behaviour.
This paper presents one such emerging symbiotic relationship:
Plant volatiles play important roles in attraction of certain pollinators and in host location by herbivorous insects. Virus infection induces changes in plant volatile emission profiles, and this can make plants more attractive to insect herbivores, such as aphids, that act as viral vectors. However, it is unknown if virus-induced alterations in volatile production affect plant-pollinator interactions. We found that volatiles emitted by cucumber mosaic virus (CMV)-infected tomato (Solanum lycopersicum) and Arabidopsis thaliana plants altered the foraging behaviour of bumblebees (Bombus terrestris). Virus-induced quantitative and qualitative changes in blends of volatile organic compounds emitted by tomato plants were identified by gas chromatography-coupled mass spectrometry. Experiments with a CMV mutant unable to express the 2b RNA silencing suppressor protein and with Arabidopsis silencing mutants implicate microRNAs in regulating emission of pollinator-perceivable volatiles. In tomato, CMV infection made plants emit volatiles attractive to bumblebees. Bumblebees pollinate tomato by ‘buzzing’ (sonicating) the flowers, which releases pollen and enhances self-fertilization and seed production as well as pollen export. Without buzz-pollination, CMV infection decreased seed yield, but when flowers of mock-inoculated and CMV-infected plants were buzz-pollinated, the increased seed yield for CMV-infected plants was similar to that for mock-inoculated plants. Increased pollinator preference can potentially increase plant reproductive success in two ways: i) as female parents, by increasing the probability that ovules are fertilized; ii) as male parents, by increasing pollen export. Mathematical modeling suggested that over a wide range of conditions in the wild, these increases to the number of offspring of infected susceptible plants resulting from increased pollinator preference could outweigh underlying strong selection pressures favoring pathogen resistance, allowing genes for disease susceptibility to persist in plant populations. We speculate that enhanced pollinator service for infected individuals in wild plant populations might provide mutual benefits to the virus and its susceptible hosts.
Cucumber mosaic virus, an important pathogen of tomato, causes plants to emit volatile chemicals that attract bumblebees. Bumblebees are important tomato pollinators, but do not transmit this virus. We propose that under natural conditions, helping host reproduction by encouraging bee visitation might represent a ‘payback’ by the virus to susceptible hosts. Although tomato flowers can give rise to seed through self-fertilization, bumblebee-mediated ‘buzz-pollination’ enhances this, increasing the number of seeds produced per fruit. Buzz-pollination further favors reproductive success of a plant by facilitating pollen export. Mathematical modeling suggests that if self-fertilization by infected plants, as well as pollen transfer from these plants (cross-fertilization) to surrounding plants is increased, this might favor reproduction of susceptible over that of resistant plants. This raises the possibility that under natural conditions some viruses might enhance competitiveness of susceptible plants and inhibit the emergence of resistant plant strains. We speculate that it may be in a virus’ interest to pay back a susceptible host by enhancing its attractiveness to pollinators, which will likely increase fertilization rates and the dissemination of susceptible plant pollen and may compensate for a decreased yield of seeds on the virus-infected plants.
Groen SC, Jiang S, Murphy AM, Cunniffe NJ, Westwood JH, Davey MP, et al. (2016)
Virus Infection of Plants Alters Pollinator Preference: A Payback for Susceptible Hosts?
PLoS Pathog 12(8): e1005790. doi:10.1371/journal.ppat.1005790
Copyright © 2016 Groen et al. Reprinted under Creative Commons Attribution (CC BY 4.0) license.
Basically, although the plants are stunted by the virus and the fruits are smaller, the likelihood of being pollinated is enhanced because the virus makes the flowers more attractive to bees. Any tendency to develop resistence will now be disadvantageous to the tomato! But the interesting thing is that it is not actually the bumblebee which distributes the virus so much as an aphid. The bumblebees 'role' is merely to be differentially attracted to the infected flowers and so differentially spread the genes for susceptibility over those for any possible resistence.
Now, to contrast the obvious evolutionary explanation for this system, what would be the intelligent (sic) design explanation? If this putative designer wants the virus to succeed for whatever reason, why not just ensure tomato plants never become resistant? Why create a virus which stunts tomato plants and reduces the yield of tomatoes in the first place when it could have designed a virus which had no detrimental effect on the plants? In short, why create the potential for an arms race and then design something to minimise the likelihood of one developing?
Can creationists come up with a scientific explanation for this system which doesn't need them to invoke mysteries and magic and entities which don't need to be proven with motives which can't be understood?
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