A new study by researchers at the Wellcome Trust Sanger Institute has revealed that the bilharzia-causing parasite, Schistosoma mansoni, made its way to the New World by travelling trough slave traders, who were first infected as they fished in the lakes of East Africa throughout the 16th to 19th century. The team examined the full DNA sequences of S. mansoni parasites from both Africa and the French Caribbean to pinpoint its origins, map its transmission across the world and determine why it was so successful.
S. mansoni is a blood fluke that infects over 250 million people worldwide and leads to more than 11,000 deaths per year. The current study used the parasite's genome, which was published by the Sanger Institute six years ago, to compare the genomes of the various S. mansoni parasites collected from across Africa and the New World. Comparing of the differences between the S. mansoni, which infects humans, and its close relative S. rodhani, which infects rodents, the team was able to pinpoint a common ancestor of the two species in East Africa between 107,000 to 148,000 years ago.
"The timing of the separation of the two species coincidences with the first archaeological evidence of fishing in Africa," Thomas Crellen, first author of the study, said in a press release. "The parasite develops in freshwater and infects people by burrowing through their skin. The introduction of fishing would have meant that people spent more time in the water, greatly increasing their chances of being infected."
Furthermore, the genome comparisons revealed that the West African parasites split from their Caribbean counterparts around 1117 AD and 1742 AD, which overlaps with the Century Atlantic Slave Trade that took place from the 16th to 19th century. During this period, over 22,000 Africans were carried from West Africa to Guadeloupe on French slave ships and they carried the parasite with them.
The study also revealed the key to S. mansoni's success - over time, certain genetic variations were positively selected over time, variations that allowed the parasites to enable them to successfully infect and thrive within humans.
"When we looked for the differences between human-infecting S. mansoni DNA and its rodent infecting cousin S. rodhaini, we found two important variations. We found that changes to two genes in S. mansoni's DNA - VAL21 and an elastase gene -appear to be important in allowing the fluke to enter and live in humans," said James Cotton, senior author of the study. "VAL genes produce proteins that cause allergic responses, so it is possible that the variation in VAL21 helps the fluke to hide from our immune systems. The elastase gene helps the parasite to burrow in to the body, by breaking down elastin - a major component of human skin."
The findings were published in the Feb. 16 issue of Scientific Reports.
