|
 The researchers said their work also deepens understanding of a
process known as zoonosis - when a pathogen that can infect animals
acquires genetic changes enabling it to infect humans - as has been
the case with diseases such as flu and Ebola.
In the case of the most deadly form of the malaria parasite,
Plasmodium falciparum, this analysis found that it gained its
ability to infect human blood cells from a section of DNA that had
transferred from a gorilla parasite.
By analyzing the crucial DNA sequence, the researchers found it
included a gene that produces a protein called RH5 which binds to a
protein receptor in human red blood cells.
"The fact that this ancestral RH5 protein was able to bind to red
blood cell receptor(s) ... from both humans and gorillas immediately
provided a molecular explanation for how P. falciparum evolved to
infect humans," said Francis Galaway, who co-led the research team
from Britain's Wellcome Sanger Institute and France's Montpelier
University.
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Malaria is spread by mosquitoes and infects around 216 million
people a year worldwide, according to World Health Organization
(WHO) data. The disease kills more than 400,000 people a year, the
vast majority of them babies and children in the poorest parts of
Africa.
"In the history of mankind, it's been estimated that malaria has
been responsible for more human deaths than any other disease," said
Gavin Wright, who co-led the work.
"So it is both important and fascinating to understand the molecular
pathways that enabled this deadly parasite to infect humans."
(Reporting by Kate Kelland and Stuart McDill, editing by Cynthia
Osterman)
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