In a vertebrate host, malaria parasites may react to coinfection by investing in growth rather than transmission to gain a competitive edge. This form of phenotypic plasticity - where a pathogen reacts to environmental changes within an infected host – is known to occur in a number of diverse pathogens. There is less understanding of whether pathogens can react to environmental changes outside their host. When might we expect such phenotypic plasticity to arise and in what form? This tantalising question was the topic of Prof. Sylvain Gandon’s seminar. It was addressed through studies in two very different types of pathogen, malaria parasites and bacteriophages.
We began with malaria, and models were used to build the hypothesis: malaria parasites, within a vertebrate host, can increase their investment in transmission when the number of mosquitoes goes up. The modelling demonstrated that there is a selection pressure for such plasticity in strongly seasonal climates due to the temporal variation in vector density. If it exists, this complex parasite behaviour may have important implications for the human malaria parasite Plasmodium vivax, which can persist in a human host in a latent state for months between episodes of growth and transmission. Using P. vivax data from around the world, we were shown a figure demonstrating a clear negative correlation between ‘length of winter’ (a proxy of strength of seasonality) against ‘investment of transmission’ (measured as the propensity of the parasite to relapse). This pattern indicates that seasonality is likely to drive lower investment in fixed transmission strategies in P. vivax. Could seasonality also select for plastic transmission strategies? To answer we need to study investment in malaria transmission under different experimental treatments, with or without exposition to mosquito bites. Fortunately, Prof. Gandon and his team have been doing just this, using birds that are susceptible to avian malaria. The results thus far do indeed support the existence of a link between parasite behaviour within the host and the mosquito biting rate.
The second half of the seminar asked whether bacteriophages can alter their mode of reproduction between lysis and lysogeny in response to the multiplicity of infection (MOI). This was inspired by a paper from 1967 (Bode) showing that lysis is inhibited to a degree that increases with MOI. Prof. Gandon again used models to suggest an answer: it is advantageous for a phage to delay lysis, and reproduce by lysogeny instead, if and only if the concentration of phage outside the cell is high. Therefore, there is a selection pressure for phages to respond plastically to MOI outside the cell. Two other examples of phages that appear to demonstrate such plasticity are the lambda phage, and the SPbeta phage.
This is exciting stuff, raising intriguing questions of any pathogen that might exhibit this kind of plasticity. How does the pathogen detect the cue? Does the extent of plasticity vary between environments (e.g. that differ in seasonality)? How reliable and specific is the cue (e.g. is the malaria response sensitive to non-vector mosquito species)? It will be fascinating to know if these kinds of phenotypic plasticity occur in human pathogens such as P. vivax. This was a highly stimulating seminar and our thanks to Prof. Gandon.
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Dr Ace North is a post-doc working on the population dynamics and control of Anopheles mosquitoes.
