Saturday, 12 March 2011

Don't (just) blame the aphids!

I spend a certain amount of time working with and thinking about aphids (AKA greenfly, blackfly, plant lice…) and have to admit to a certain amount of affection for them. I doubt that many farmers and gardeners feel the same way as they are significant pests of most crops and many garden plants. One of their most serious effects is through the transmission of plant viruses as these can cause massive economic damage to crops (eg BYDV, PVY). Note I am not getting into the different virus transmission types (persistent, semi-persistent and non-persistent), but you can read about the differences here. The discussion below is about a non-persistent virus. 

Although it is the virus that causes the damage it is generally the aphid that is seen as the villain in this scenario and it is always the aphid that is the target of any control options.  Often all aphids are seen as a problem, even if only a small number of species (there are over 500 in the UK alone) are actually capable of transmitting a particular virus. At the most basic level, the aphid picks up the virus by feeding on or tasting an infected plant, then moves to another plant and transmits the virus by feeding/tasting again. I think it is often assumed that the virus is passive in this process and that the aphid [maliciously?] skips around spreading as much virus as possible.

However, the relationship between the virus, the plant and the vector is always a complex one that has been shaped over time by natural selection. A number of investigations have shown that, in some plant-virus-vector relationships at least, it is the virus that manipulates the situation to maximise it’s chances of being spread between plants. A relatively recent example is that of the Cucumber mosaic virus and two aphid species Myzus persicae and Aphis gossypii (Mauck et al, 2010). They have shown that the aphid is attracted to infected plants to pick up the virus and then repelled from those plants leading to an increased likelihood of transmission to a healthy plant.

So, how does this work?
  1. The virus in an infected plant
    1. Affects the nutritional balance of the plant so it is not a good host for the aphids
    2. Affects the plant chemistry so that the volatiles escaping from the plant suggest that it is an extremely good host for the aphids
  2. The aphid arrives in the field
    1. Uses plant volatiles to find suitable hosts leading to a good chance that they will land on an infected plant as the plant is giving the signal of ‘very good host’
    2. Once they have landed and tasted the plant (picking up the virus) the actual nutritional balance of the plant suggests it is not a good host and there is a good chance that the aphid will fly of in search of another, more nutritious plant.
    3. Eventually they will come across a good host, which is likely to be an uninfected plant and transmit the virus to a new host.
So the manipulation of the plants biochemistry by the virus essentially tricks the aphid into giving it a ride to healthy plants where it can multiply and continue the process.

There is (probably) nothing in this for the aphid – it is just a dupe, and ultimately not to blame!

This shows that, as with many biological relationships (and indeed many other things), what may appear simple on the surface can actually be a much more complex situation once the detail is investigated.

Reference: Mauck KE, De Moraes CM, Mescher MC. 2010. Deceptive chemical signals attract insect vectors to inferior hosts. Proc Natl Acad Sci 107 (8): 3600–3605. [LINK]


  1. Thank you for very interesting post.

  2. Hi Phil,
    this is an interesting post and paper by Mauck et al - thanks for pointing it out! Ive looked into this quite a bit for the project Im doing and there is a lot of controversy in the literature on some of these plant-insect-virus interactions. The colour of virus infected plants is thought to attract aphids (Ajayi B.O., 1983;Medina-Ortega, 2009). This may be quite complex, as after becoming viruliferous, apterae then showed no preference between virus-infected and noninfected plants (Medina-Ortega, 2009). However, others have found the opposite to be true: R. padi has been found to prefer healthy barley leaves over BYDV-infected ones (Kieckhefer, 1976), the same was found on oats (Power, 1996).
    I also think there is a lot to explore with the impacts of YDVs on Morphology – BYDV can lead to an increase in alate formation (Gildow, 1980): With around 500 aphids maturing in each treatment, the percentage of R. padi developing as alateae on healthy oats, RPV-infected oats, and MAV-infected oats was 35, 74 and 81, respectively. Similar to results found for S. avenae in the same paper. This effect may depend on the stage of BYDV infection, with the early stages probably producing more alates – based on research with Zucchini yellow mosaic virus (Blua, 1992). However, this may be the result of a ‘trade-off’ between the virus causing increased alates whilst the plant is relatively healthy with greater symptom formation on the plant in later stages reducing this effect? This effect may be linked to increased fecundity and attraction of the aphids to BYDV infected plants in early stages, so that really it is just a result of higher aphid densities rather than a physiological phenonemen (Medina-Ortega, 2009).
    Altogether a really interesting area to investigate, and with the impacts of climate change it is difficult to know what implications there may be for the spread of the virus - this is the question we trying to address in our project.