For an organism to become a parasite it has to adapt to live in a host. This might mean it needs to grow faster, invade cells or tissues, or avoid being killed by the immune system. It can also 'forget' how to live outside a host. It can forget how to search for food, how to survive the cold, and how to avoid drying out.
We can learn how parasites adapt to infect hosts by looking at the nearest free living relatives. What had the parasite lost relative to the free living cousin, because it just doesn't need it to survive in a host? Or vice versa
, what has it kept because it's useful for infecting a host?
I've looked at this question for trypanosomatid parasites. They are protozoan (single cell) parasites, like the malaria parasite, and cause several deadly tropical diseases.
A few hundreds of millions of years ago, they weren't parasites at all. The ancestors of these parasites were free living, probably swimming in ponds, lakes and seas. Then, at some point, some evolved the ability to infect insects.
Millions of years passed. Then, several tens of millions of years ago, some managed to get transmitted from their host insect into a vertebrate host. And, most importantly, they survived and could get transmited back to the fly.
This adaptation to infect animals probably happened on three separate occasions. Those parasites kept evolving and adapting, and are now the three human trypanosomatid-caused diseases: Sleeping sickness, Chagas disease and leishmaniasis.
My most recent paper is all about this. Julius Lukeš has discovered a species of trypanosomatid that only infects insects, and looks like it hasn't changed much from the first ancestor ever to infect insects.
With Tomáš and Eva, we looked at what this species tells us about how these parasites adapted to infect flies: How does the cell grow, adapts its shape, and stick to surfaces? How does its internal organisation adjust to allow these changes? How does its metabolism change for different energy sources? And, how has the genome, which encodes the proteins that drive these functions, changed to achieve this?
Using this information, we could then get insights into what is important for human infective parasites. What aspects of shape, structure and metabolism adaptations have they 'forgotten'? And which have they kept? The ones they have kept are the ones important for infecting, and killing, people.
Want to read more? You can get a copy of the paper from my website: richardwheeler.net
Skalický T*, Dobáková E*,1, Wheeler RJ*, Tesařová M, Flegontova P, Jirsová D, Votýpkaa J, Yurchenkoa V, Ayalag FJ, Lukeš J (2017) "Extensive flagellar remodeling during the complex life cycle of Paratrypanosoma, an early-branching trypanosomatid" PNAS doi:10.1073/pnas.1712311114