Contributed by Guest Blogger: H. Tran ‘14
A virus’s ability to replicate is largely dependent on the health of its host; a virus cannot proliferate in an immobile or dead organism. For this reason, viruses have a vested interest in doing as little damage as possible to ensure easy transmission. Vector-borne pathogen transmission between plants is seemingly ideal for viruses as particles can move freely from one diseased host to another potential host. However, infected plants do not typically attract vectors in the first place, as they don’t promise healthy feeding. One common crop virus is able to sidestep this obstacle by causing its diseased host to release a greater number of vector-attractants without sacrificing virulence.
It was recently discovered that the widespread plant pathogen cucumber mosaic virus elevates the release of host volatiles, or odorous chemicals, that attract vectors. Researchers measured the rates of aphid population growth on and emigration from healthy and infected plants. It was discovered that aphids were initially more attracted to the infected plants than to the healthy plants. However, the aphids dispersed rapidly from the diseased hosts after feeding. This form of transmission is known as non-persistent transmission because rather than long-term feeding and colonizing on the plants (persistent), the vectors are repelled by the inferior quality and move on to other plants (non-persistent). This type of transmission is advantageous for CMV as it facilitates easy transmission from one host to another.
It is known that the non-persistent nature of CMV transmission encourages quicker spreading between host and uninfected plants. It remains unclear, however, whether the elevated level of volatile emission is a result of an adaptation to hosts for the purpose of manipulating vectors or simply an accidental by-product of infection. In either case, the phenotypic change resulting in higher levels of volatile release has the capacity to significantly alter ecology, agriculture and human health. Damaged crops are less nutritious and unmarketable, making CMV a vastly undesirable pathogen.
Which is a more probable explanation for the deceptive mechanism by which the virus enhances host-vector interaction: manipulative adaptation or coincidentally advantageous evolution? What does your conclusion tell us about the evolution of this virus, or viruses in general? Knowing what was recently discovered about CMV, can anything be done to prevent the cultivation of diseased crops?