Why study disease across biological scales?

To understand the evolutionary biology of infectious diseases, we need to study both within-host (e.g., immunological) and between-host (e.g., transmission-related) processes. Why? We must study both scales because we know that parasites must succeed on both scales if they are going to spread and persist in host populations.

The logic is as follows. A parasite that outwits its host and escapes clearance by the immune system can only be successful evolutionarily — i.e., can only gain genetic representation in the next generation of parasites — if it is also transmitted from one host to the next. In other words, immune escape that leads to a transmission dead-end will get a parasite nowhere! And conversely, a parasite that excels at transmission (traveling from one host to the next, whether via a sneeze or an insect vector) yet fails to survive immune attack in the next host will also be an evolutionary dud.

So we as scientists must understand parasites across the whole life cycle if we are to understand and predict the evolution of parasites over time and in response to medical interventions.

Philosophical Transactions of the Royal Society special issue now published!

There is growing recognition that the development of new, evolutionarily robust treatments and interventions against infectious disease requires a better understanding of the dynamics of parasites and pathogens inside their hosts. While progress in microbiology and immunology has continued to unravel complex molecular interactions between microbes and their hosts, population biologists have begun deploying new tools to understand the ecological causes and evolutionary consequences of the observed within-host dynamics. In particular, this work has formalised the dynamics of infection to enable quantification of the relative roles of target cell limitation and immune responses in controlling infection within a host. Such a framework, in turn, generates testable predictions about which parasite or pathogen genotypes will have a competitive advantage within hosts and thus will be transmitted across the host population. Theoreticians took the step from within-host dynamics to between-host transmission many years ago, but their models are only now beginning to be tested and improved, thanks to new developments in both experimental and statistical techniques.

To build upon and promote these developments, several RCN members (led by Olivier Restif and Andrea Graham) contributed to the current issue of Philosophical Transactions of the Royal Society, Within-host dynamics of infection: from ecological insights to evolutionary predictions.


A biofilm of Vibrio cholerae

Multiple colored variants of a strain of Vibrio cholerae (a causative agent of cholera in human hosts) co-inoculated on glass. The variants express 3 different fluorescent proteins that enable visualization of the contribution of each to biofilm formation. One optical slice at the base of a biofilm is shown in two of these images, while the 3-D volume snapshot was rendered using a z-stack of optical slices of the biofilm.  Biofilm formation can affect virulence and persistence of this important human pathogen.

Long-tailed macaques in Borneo

These monkeys host arboviruses as well as the primate malaria species Plasmodium knowlesi which can also infect humans.  Key determinants of whether macaques and people share parasites include proximity of human habitation to the forest, the location and feeding preferences of mosquito vectors, and relative susceptibility of the host species.  Zoonotic reservoirs like these can play a major role in the evolution and persistence of parasites. And for species of conservation concern, parasites can have an important effect on likelihood of extinction.