Before working on plague, I worked on HIV and chlamydia, two common sexually transmitted diseases.
For HIV, I explored how the human immune system could keep up with a fast-evolving pathogen that only recently (somewhere after 1900) spilled over into human populations.
In two papers1,2, we found that the genetic variation in humans stopped HIV from adapting to all of us. The next step was to understand this process for pathogens in general3 and whether the current setup of our immune system was a natural consequence of evolutionary pressure4.
For my research on the spread of chlamydia, I created a simulation of the sexual network of the Netherlands5. Finding a model description that mimicked the real network well enough was quite a challenge!
Like the COVID modeling in 2020-2022, we used this model to simulate disease spread and the effect of various interventions and compare the results to the impact we saw in actual intervention programs.
Schmid, B.V., Keşmir, C. and de Boer, R.J. (2008) The specificity and polymorphism of the MHC class I prevents the global adaptation of HIV-1 to the monomorphic proteasome and TAP, PLOS ONE.
Schmid, B.V., Keşmir, C. and de Boer, R.J. (2009) The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes, BMC Evolutionary Biology.
Schmid, B.V., Keşmir, C. and de Boer, R.J. (2010) Quantifying how MHC polymorphism prevents pathogens from adapting to the antigen presentation pathway, Epidemics.
Schmid, B.V. (2009) The emergence of polymorphism in the antigen presentation pathway. Chapter 5, pp. 75-84 of my PhD thesis 'Limits of viral adaptation to the antigen presentation pathway'. Utrecht University.
Schmid, B.V. and Kretzschmar, M. (2012) Determinants of sexual network structure and their impact on cumulative network measures, PLOS Computational Biology.