Comparing phylogenies of very distantly related species that share an ecological relationship is one of the classic ways to determine if coevolution is involved. https://evolution.berkeley.edu/evolibrary/article/evo_46.
An example: Gophers and lice
These and studies of interactions between species revealed complexities in the evolutionary race between parasite and host.
The race is classically described as fitting the red queen hypothesis.
However research has indicated, evidence of frequency dependent selection of traits or genes has been difficult to demonstrate. From case studies in which the evolutionary history of parasites/pathogens is well known, we gave generated at best some generalities such as virulence decreases with length of the parasite-host relationship and horizontal transfer favors increased virulence over vertical transfer.
Most influential studies for application have been serial transfer studies. Serial passage in a new strain often increases virulence there, but decreases virulence in the former host. (https://en.wikipedia.org/wiki/Serial_passage)
Also some case studies in bacteria indicate similar trends.
But a look at a classic study indicates caution.
A classic study. Australian "rabbits" and an introduced virus.
In 1950, a single strain of myxoma virus of South American rabbits (Sylvilagus brasiliensis) was released in Australia as a biological control agent against European rabbits (Oryctolagus cuniculus). Frank Fenner, realizing this would be a grand experiment in virulence evolution, set in motion a series of experimental studies to monitor the subsequent evolution of viral virulence. These studies involved measuring the lethality of virus isolates taken from the field in standardized laboratory rabbits. The work showed that the original highly lethal strain, with a case fatality rate (CFR) of close to 100%, was rapidly replaced by strains with case fatality rates of 70–95% or lower, and sometimes even less than 50%. Fenner and colleagues then went on to show that this attenuation was favored by natural selection because, by killing hosts so rapidly, highly virulent viruses had shorter infectious periods than more attenuated strains, which did not kill so rapidly. This work became the bedrock of the mathematical theory of virulence evolution developed in the 1980s , and it remains so because the combination of temporal field sampling and controlled experimentation demonstrating the relevant trade-offs is unique for a disease of vertebrates.
However, newer a 2017 from which the previous paragraph was taken warns of new virulence in the virus at least based on 1990 samples. https://www.pnas.org/content/114/35/9397 This new work stresses that the evolutionary advantage because of shorter generation time and larger populations size goes to the parasite or pathogen. It also introduces the possibility of problems that could arise out of changing of host immune strategies as in adding genes for resistance.
We have begun to study how changes in the environment have caused changes in parasite response.
"Life history theory has been applied to the allocation of resources between the growth and transmission stages during the blood stage of malaria infections [4,12,13]. The optimal allocation of resources between growth and transmission stages may change in environments that increase the mortality of the parasite, such as after the generation of immunity during the course of an infection, or after drug treatment. At high levels of mortality, when extinction of the parasite is certain, the parasite should invest mainly in the transmission stage. At low levels of mortality, the parasite should increase allocation into the growth stage as this prevents clearance of the parasite. An interesting recent study by Reece et al. applied these ideas to drug treatment by proposing that the parasite should display adaptive phenotypic plasticity in response to the severity of the treatment [5]. At high drug doses the parasite should increase investment in the transmission stage, consistent with earlier in vitro observations [14,15]. At low drug doses the parasite should decrease investment in the transmission stage, and they demonstrated this to be the case in an in vitro setting. from Parasite Evolution and Life History Theory Beth F. Kochin et al., PLoS Biol 8(10): e1000524. doi:10.1371/journal.pbio.100052"
Unfortunately such flexibility has led to a pattern of mosaic evolution that for the most part simply complicates the picture now, but may yield insights in the future.https://en.wikipedia.org/wiki/Mosaic_coevolution
Recent studies have also led to suggestions of combating rising immune disease and allergies with Helminth therapy.
History:
The term "hygiene hypothesis" to describe one of the causes of inflammatory disease in Western culture. David Barker coined the term in 1988 and used the term to explain an increasing incidence of appendicitis in rural communities. Barker provided a potential explanation for an increased incidence of appendicitis. Barker's explanation for appendicitis utilized the widely held view in 1988 that the primary problem leading to allergic disease was delayed exposure to infectious agents. According to that model, exposure to infectious agents relatively late in life caused immune disease
https://en.wikipedia.org/wiki/Helminthic_therapy
The hygiene hypothesis has changed to the biota alternation hypothesis because of what we know now about how our immune system reacts to helminths
What do we know about how parasites regulate the immune system?
The reactions are complex, involve the innate immune system which has been little studied and relationships evolved so long ago.
Of the 223 identified parasitic origins, 186 (83%) occur at or below their present taxonomic rank of family and 113 (51%) occur at or below the level of genus. However, 90% of parasite species diversity occurs in the 10 largest parasitic clades, all of which appeared prior to the Mesozoic https://s/10.1371/journal.ppat.1003250
Host:
The response to worms involves both systems.
A key component of the immune system that has evolved to minimize the virulence of helminths is the type 2 (or TH2) response. Instead of giving us allergies and asthma, the type 2 response likely evolved both to provide resistance by limiting the number helminths that can live in our intestinal tract and to repair the tissue damage that is caused by the helminths that have colonized our tissues. It appears the immune system in general is ineffective in preventing worm colonization, but effective at preventing secondary infections and counteracting worm damage. The response is characterized by the production of cytokines such as interleukin-4 (IL-4), IL-5, IL-9, and IL-13. Signaling through interleukins and other cytokines in intestinal epithelial cells promotes goblet cell differentiation and increases mucus production, as well as increases proliferation and turnover of these cells.
This may help also maintain the mucosal barrier and limit aberrant responses triggered by the gut bacteria. In fact, some researchers point out some of this response may have even evolved in response to maintaining a healthy relationship with various bacteria. Increased contraction of intestinal muscles and the activation and release of mast cell products that can increase fluid flow into the lumen may also help flush the worms out of the gut. Other cells involved in tissue repair also are activated by cytokines such as macrophages,basophils, eosinophils, and mast cells which also produce more cytokines that amplify the response. The absence of this type 2 response during helminth infections in mice is often associated with lethal sepsis from compromised gut integrity and leakage of gut bacteria.
Other work has indicated that this response is important in regulating inflammation damage in prolonged infections and wound healing. Severe systemic stress, immunosuppression, or overwhelming microbial inoculation causes the immune system to mount a type 2 response to an infection normally controlled by type 1 immunity.
Overall, the prevailing pattern is that there are few commonalities between the genomes of independently evolved parasitic worms, with each parasite having undergone specific adaptations for their particular niche.
Overall, it appears that antigenic variation of proteins is not a common method in helminths of avoiding the host immune system, and maintaining a chronic infection. Instead, the parasitic worms are using a range of different strategies; minimizing its exposure to the host immune system through encapsulation and other surface modifications and manipulating the host immune system through secretions of immunomodulatory agents. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413821/
So it is these manipulative chemicals that our immune system would target, unfortunately these are secreted well after the worm colonized our tissues.
In summary, the worms have evolved to provide little for our immune system to respond to until after the worms have set up shop so to speak. Are we seeing more in the way of allergies and auto-immune diseases simply because the worms are gone? Probably not. The worms have evolved to regulate the system that minimizes their effects and initially may have been more effective in their expulsion. This system also mediates the effects of bad bacteria, involved in wound healing and cell turnover and comes into play later in chronic infections. It is a maintenance system that is making mistakes in what it attacks probably because of the different internal and external stress placed on our bodies due to modern life. Worms can help us regulate this system and right now they seem to be an easier fix than other choices. However we should not forget, a worm infection comes with associated costs.