A new study shows that the malaria species widespread in the
Asia-Pacific region has been a key driver of human genome evolution.
Malaria is a parasitic disease
with devastating effects, causing up to one million deaths annually worldwide.
Approximately half the world’s population is at risk of malaria infection. The
disease is a major cause of poverty and has been a barrier to economic development.
The most prevalent malaria
species in the Asia-Pacific region is Plasmodium vivax, widely considered to be
a ‘benign’ form of malaria.
In comparison, Plasmodium
falciparum is the species that causes the most severe disease and deaths from
malaria. For this reason, P. falciparum has been thought to be the most
important driver of human genome evolution.
An international team of
researchers now report in PLoS Medicine that the milder P. vivax species is
also a significant cause of genetic evolution, which provides protection
against malaria.
The team who made this discovery
included scientists from the Papua New Guinea Institute of Medical Research and
the University of Western Australia, and was led by Professor Ivo Mueller from
the Walter and Eliza Hall Institute of Medical Research in Australia.
Early on, the researchers
observed that the incidence of a hereditary red blood cell disorder was
unusually high in the Asia-Pacific region.
Southeast Asian ovalocytosis
(SAO), indigenous to Malaysia and Papua New Guinea, is a condition caused by a
genetic defect in a cell membrane protein that results in red blood cells being
a different shape from normal.
Up to 35 percent of inhabitants
along the coasts of Papua New Guinea carry this genetic defect. Because these
are high malaria endemic areas, it is believed that SAO could be associated
with improved survival against malaria.
“SAO occurs in approximately 10
to 15 percent of the population in parts of the South West Pacific and is
caused by a hereditary mutation in a single copy of a gene that makes a red
blood cell membrane protein. This is almost an absurdly high frequency when you
consider that inheriting two copies of the mutation is invariably fatal, so we
figured it must confer a strong advantage to the carriers,” said Mueller.
The researchers studied 1,975
children, from infants to 14 years of age, in the Madang area of Papua New
Guinea. The incidence of infection by the malaria parasites P. vivax and P.
falciparum was significantly reduced in SAO-positive children, while the risk
of infection was reduced between 46 and 55 percent, depending on the age of the
children.
“Humans and malaria parasites
have been co-evolving for thousands of years,” Mueller said. “Malaria has been
a major force in the evolution of the human genome, with gene mutations that
provide humans with some protection against the disease being preserved through
natural selection because they aid in survival.”
Controversially, this finding
goes against the established theory that P. falciparum, responsible for the
most lethal form of malaria, is the only malaria parasite that can drive genome
evolution in humans.
“Our results suggest that P.
vivax malaria, though until recently widely considered to be a ‘benign’ form of
malaria, actually causes severe enough disease to provide evolutionary
selection pressures in the Asia-Pacific,” explained Mueller.
Prof. Mueller expects these
findings to impact malaria vaccine design and development.
“Studying the mechanisms that
cause SAO-positive people to be protected against P. vivax malaria could help
us to better understand the mechanics of infection and help us to identify
better targets for a malaria vaccine,” he said.
The article can be found at: Rosanas-Urgell A et al. (2012) Reduced Risk of
Plasmodium vivax Malaria in Papua New Guinean Children with Southeast Asian
Ovalocytosis in Two Cohorts and a Case-Control Study.
Source: WEHI
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