Social environments and disease transmission; from individuals to populations
Dr Amanda Bretman (SOB), Dr Steve Sait (SoB)Contact email: email@example.com
An increasing body of evidence shows that fine scale social structure is having widespread ecological and evolutionary consequences (Kurvers et al 2014). A particularly important component in terms of individual fitness, population stability and demography is the spread of infectious disease, which is intrinsically linked to social environments and behaviours that lead to disease transmission between individuals (Chambers and Schneider 2012). These patterns are not always clear cut, and there is as yet no consensus on how group size or social connectedness determine infection rate (Salazar et al 2016). This may be partly because prophylactic strategies such as up regulation of immunity-related genes (Cole 2013) and sickness behaviours (Loehle 1995) enable even highly social connected animals to predict and reduce the risk or severity of infection. Furthermore, disease risk often changes as individuals age. Juvenile social environments might also be dominated by competition for resources and foraging behaviour that increase disease risk, whilst adult social environments might be dominated by reproduction and behaviours that leads to contact between mates.
Effects of social environments are much more widespread than in animals classically thought of as “social”. The longstanding laboratory model species Drosophila melanogaster fruit flies are sensitive to social contact in a variety of ways, from larval cooperation (Rohlfs and Hoffmeister 2004), to the amount they sleep (Donlea et al 2014), to their reproductive tactics (Bretman et al 2009). We have previously shown that males live longer if they are isolated (Bretman et al 2013) and we have recently extended this to reveal that Drosophila melanogaster fruit flies show sex-specific outcomes in terms of the effects of the interaction between wounding, social contact and survival. Pairing reduced lifespan but this was more severe for males, and this effect doubled if the flies were immune-challenged. Intriguingly, we have also found that social contact actually increases survival after being infected with a lethal pathogen.
This project will build on these discoveries to investigate how immune response and disease spread are affected by more complex social environments. For example, given the trade-off between immune responses and reproduction (Schwenke et al 2016), whether the effect of social contact interacts with the costs of mating. Likewise, as fruit flies are often found in multispecies groups, we need to determine whether interspecies contact has similar effects as intraspecies interactions. This will develop the complexity of our model to more accurately reflect natural ecological conditions within a strictly controlled laboratory environment. In addition, fruit flies are known to have a genetically determined preference for different types of social environments (Saltz 2011) and this affects, for example, how aggressive they are when housed in groups (Saltz 2013). Changeable environments may therefore lead individuals to find themselves in unfavourable social contexts. This gives us the ability to determine the consequences of dynamic social environments, both for the individual’s ability to mount a costly immune response and for the transmission of disease.
Bretman et al 2009 Proc R Soc
Bretman et al 2013 Evolution
Chambers and Schneider 2012 Curr Opinion Immunolgy
Cole 2013 Am J Public Health
Donlea et al 2014 Sleep
Kurvers et al 2014 Trends Eco Evo
Loehle 1995 Ecology
Rohlfs and Hoffmeister 2004 Oecologia
Salazar et al 2016 PLoS One
Saltz 2011 Evolution
Saltz 2013 Proc R Soc
Schwenke et al 2016 Ann Rev Entomol
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