Heritability of susceptibility to disease in the wild
Measures of heritability for disease susceptibility in wild populations are relatively rare: for example, only between 0.03 and 2.5% of studies of heritability estimates of traits in wild populations were related to disease . However, some recent studies have found that there may be considerable additive genetic variation associated with disease susceptibility in the wild. For instance, heritability of infection risk was found to be 12% for Mycobacterium bovis in adult European badgers and 55% for Mycoplasma ovipneumoniae in bighorn sheep . Interestingly, we found relatively low environmental effect variance for disease in this population, explaining less than 1% of the total variance. The low shared-environment effect variance found here may reflect the small size of the study area that this population inhabits (of only 13 km length, and several hundred meters width), and therefore relative homogeneity in environmental conditions for all koalas. Nevertheless, considerable variation in susceptibility to disease remains unexplained (in the residual variance), suggesting that there are other environmental factors influencing disease in this population that were not captured by the shared environment effect. Moreover, additive genetic effects in disease are likely not homogeneous across ages . We were not able to formally investigate this, owing to low statistical power at different ages, but this would be an interesting and valuable follow-up study.
Narrow sense heritability (h2), as calculated in this study, can be used to predict the response to selection across generations (Walsh and Lynch 2018), and can therefore be used to predict outcomes for populations facing disease outbreaks . Heritability is a population-level parameter which depends on population-specific factors (e.g., allele frequencies or the effects of gene variants), traits, and variation due to environmental factors . Together with recent findings suggesting that polymorphisms in immune genes play an important role in koalas’ ability to resolve a chlamydial infection , the additive genetic variance for susceptibility to infection suggests there may be some potential for koalas to respond adaptively to the presence of the pathogen. Given the degree of heritability found in this population, the immediate question is why have koalas in this population not yet adapted to be resilient to chlamydia?
There are several possible reasons for the maintenance of genetic variance in disease susceptibility in this population. First, genetic variance may be maintained through antagonistic pleiotropy with traits associated with other fitness components . Second, predation (predominantly by dogs) accounted for about 63% of all mortality in this population and could therefore have imposed a stronger selective pressure than disease. Third, koalas are hypothesized to have both their own chlamydia species and others more recently transmitted from livestock over the last 200 years (Timms 2005), so – whilst there is not yet any empirical support for this hypothesis – a possible explanation for the current virulence of chlamydia is that new strains have recently been introduced, and there has not been sufficient time for adaptation of resistance to these new strains. Finally, pathogens also adapt in response to host resistance and/or tolerance, and theoretical models suggest that maintenance in genetic variation in resistance to pathogens may be explained by a continuous process of host-pathogen coevolution .