Human niche-constructing activities may inadvertently promote disease. Cultural practices, such as cultivating crops and keeping animals, appear to have aided the spread of diseases, such as malaria and sickle-cell anaemia, leading to the selection of alleles that confer resistance to the promoted diseases (Durham 1991; Laland et al. 2010; O’Brien & Laland 2012).
Many human genes that provide some immunity from, or resistance to, disease or pathogens are now known to have been subject to recent selection, and are thought to have been promoted by agriculture or other farming practices (Laland et al. 2010).
The inadvertent construction of disease niches by human cultural activities may have been going on for some time, and is implicated in the emergence of tuberculosis, an ancient human disease. The controlled use of fire may have triggered the spread of TB, through a combination of increased opportunities for transmission brought about by the developing social culture that fire use encouraged and the lung damage that smoke inhalation caused (Chisolm et al. 2016).
Another system that exhibits feedback between human cultural niche construction and genetic selection is the host-parasite relationship between antibiotic treatment and viability selection for antibiotic-resistant bacterial strains. This is an example of inter-specific cultural niche construction. Boni and Feldman (2005) found that the cultural transmission of antibiotic use favours selection of resistant bacterial strains, which in turn can result in cultural selection for the avoidance of antibiotic use.
This kind of host behaviour can result in the classic niche-construction phenomenon of maintaining strain polymorphism even in parameter regions where it would not otherwise be expected. Interestingly, the evolution of either the host activity or the parasite strain can be viewed as a niche-constructive activity that modifies the selective environment of the other. Potentially this promotes an arms race between two types of transmitted information, cultural and genetic.
Here, the niche constructive effects can be described fully in terms of trait–trait co-evolution as there is no ecological inheritance of a constructed ‘resource’ that is separate from the cultural or the genetic information transmission systems. The relative frequencies of bacterial resistance and sensitivity are the effective ‘resource’ influencing the cultural evolution of antibiotic treatment, and visa versa.
Disease vectors too can construct niches. For instance, as obligate parasites, viruses too are constantly modifying the host environment, and these modifications are now thought to drive evolutionary feedback between the virus and its host, across multiple scales, from cells to ecosystems (Hamblin et al. 2014). For instance, the rabies virus causes aggression of the host and thereby facilitates its own propagation.
Boni MF, Feldman MW. 2005. Evolution of antibiotic resistance by human and bacterial niche construction. Evolution. 59(3): 477–491. Explores coevolution of medicines and bacterial strains through reciprocal niche construction.
Chisholm RH, Trauer JM, Curnoe D, Tanaka MM. 2016. Controlled fire use in early humans might have triggered the evolutionary emergence of tuberculosis. PNAS. 113(32):9051–56. Discusses how controlled use of fire may have led to spread of tubercolosis
Hamblin SR, White PA, Tanaka MM. 2014. Viral niche construction alters hosts and ecosystems at multiple scales. Trends in Ecology & Evolution. 29(11): 594-9. Viruses modify host environments, and these modifications drive evolutionary feedback between the virus and its environment across multiple scales from cells to ecosystems.