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 .