Vaccines have stood the test of time; pathogens have rarely evolved resistance to vaccines and they are still incredibly effective at preventing epidemics. Yet drug resistance is a widespread phenomenon and it is increasingly difficult to manage. Why do we see this difference? CIDD’s David Kennedy and Andrew Read sought the answer to this question by applying popular resistance principles in a succinct way.
Kennedy and Read postulate that vaccines do not confer pathogen resistance because they have large, synergistic effects. Drugs are typically only administered after symptoms appear, i.e. therapeutically. By this point in the infection, the pathogen population is large and genetically diverse. Conversely, vaccines are administered prophylactically, or prior to known exposure. The immune response of the host keeps pathogen populations low and thus reduces onward transmission and the accumulation of genetic diversity. Further, vaccines expose the host’s immune system to multiple antigens and multiple binding sites on those antigens, whereas drugs target a specific step in a pathway. Thus to avoid a drug, a pathogen must evolve around one step, but to avoid a vaccine, a pathogen must acquire numerous changes (similar to combination therapy).
Together, timing of action and the multiplicity of target sites have allowed vaccines to be successful for decades (even centuries in the case of small pox). These mechanisms may be key to slowing drug resistance to chemotherapies and other important treatments.
Synopsis written by Ellen Brandell
David A. Kennedy, Andrew F. Read
Why does drug resistance readily evolve but vaccine resistance does not?
Journal: Proceedings of the Royal Society Biological Sciences