Nearly 200 Million Africans at Risk for Malaria

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New research shows that after 10 years of intensified campaigns against malaria 184-million people in Africa still live in moderate to high-risk areas. While the number is high, it’s down from nearly 220-million in 2000 when anti-malaria efforts began to increase.

The findings are based on thousands of community-based surveys in 44 African countries and territories. These are places where malaria has been endemic.

Dr. Abdisalan Noor, co-leader of the team that conducted the research, said, “What we are looking at, first of all, is to try and estimate the level of infection with malaria in African communities. This doesn’t necessarily mean the number of people who die of malaria, but the proportion of people who are likely to carry the most virulent type of the malaria parasite. That’s Plasmodium falciparum.”

Noor and co-leader Professor Robert Snow are with the Kenya Medical Research Institute-Wellcome Trust Research Program. The team also included researchers from Oxford University and the World Health Organization.

The study reflects the effects of the Roll Back Malaria campaign and other programs. The campaign brought together many multi-lateral, private and non-governmental organizations. The goal was to cut in half the number of deaths from malaria by 2010. It had a shaky start and was criticized in its early years for a lack of progress.

Dr. Noor said that the new study finds a mix of good and bad news about efforts to combat malaria.

“The positive news is there has been production in 40 of the 44 African countries for which we were able to estimate change. There has been some reduction in the proportion of people who are likely to be affected with the falciparum parasite. About 218-million people in 2010 lived in areas where transmission – malaria transmission – had dropped by at least one level of endemicity. So that’s good news.”

Endemicity is described as the measure of disease prevalence in a region.

“The other side of it.” said Noor, “is that despite all these gains almost 60 percent of African populations still live in areas where more than 10-percent of the population is likely to carry the malaria parasite. And out of these about 184-million people live in areas where more than 50-percent of the population are likely to carry malaria infections.”

Among the countries where disease transmission remained high or unchanged are DRC, Uganda, Malawi and South Sudan.

Despite the large number of people still likely to be infected, Noor says he does not want to detract from the gains made by the international community – namely, the reduction in risk for 34-million people from 2000 to 2010.

“We haven’t actually looked at the reasons why some places are more resilient to change than others. Epidemiologically, it’s got something to do with the higher the starting transmission, the longer it takes to bring down the disease,” he said.

Another reason, he said, may be weak health care systems in many countries. It can be difficult to get reliable estimates on how many people get sick or die from malaria. Noor says stronger health care systems would play a major role in reducing infection risk.

In the 10-year period studied, funding for malaria programs steadily increased from 100-million-dollars to two-billion dollars a year.

He said, “It’s no news that despite all this investment we need more. I think the estimate for the needs for malaria control in Africa is around five-billion dollars if we look at the last global malaria action plan.”

Noor said that there’s a lot to be proud of in the global community in terms of reducing malaria cases.

He added that despite a recent global recession — and competing priorities — resources for malaria campaigns should not only be sustained, but increased. That would help bring malaria to a point where, he said, it would be of “minimal public significance.”

Right now, though, the Roll Back Malaria campaign estimates a child dies every 60 seconds from the disease.

 

Source: VOA News

Researchers Show Evidence of Genetic “Arms Race” Against Malaria

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For tens of thousands of years, the genomes of malaria parasites and humans have been at war with one another. Now, University of Pennsylvania geneticists, in collaboration with an international team of scientists, have developed a new picture of one way that the human genome has fought back.

The international team was led by Sarah Tishkoff, a Penn Integrates Knowledge professor with appointments in the genetics department in Penn’s Perelman School of Medicine and the department of biology in the School of Arts and Sciences, and Wen-Ya Ko, a postdoctoral fellow in the genetics department at the medical school.  They performed a genetic analysis of 15 ethnic groups across Africa, looking for gene variants that could explain differing local susceptibility to malaria.

Malaria remains one of the deadliest diseases on the planet, annually killing about a million people, 90% of whom live in Africa. Different populations show different responses to the parasites that cause malaria; the team conducted the largest cross-population comparison ever on a pair of genes related to malaria’s ability to enter red blood cells.

“When you try to identify the variants that are associated with disease susceptibility, it’s important to do a very fine scale study,” Ko said. “Different populations evolve independently, to a certain degree, so different populations can come up with unique mutations.”

The life cycle of malaria depends on infecting red blood cells by binding to their surfaces, which is why mutations, such as sickle cell anemia, that change the overall shape of those cells are thought to have experienced positive selection.

“Both host and the parasite try to fight back with mutations; it’s a co-evolution arms-race that leaves a signature of selection on the genes,” Ko said. “We’ve identified several single-nucleotide polymorphisms that are candidates for that signature.”

Across the 15 population sets, the researchers focused on polymorphisms in a pair of genes that code for proteins called glycophorin A and glycophorin B. These proteins exist on the surface of red blood cells, and changes to their shape affect the ability of the parasite causing malaria to bind to them and to infect the cells.

There are, however, two conflicting theories of why changes to glycophorin shape influence rates of malaria. One theory suggests that glycophorin A acts as a decoy, making itself more attractive to binding so that pathogens don’t infect more vulnerable cells. Another theory suggests that glycophorin A mutates so that malaria parasites can’t bind at all.

The researchers observed differing patterns of natural selection acting on the different regions of the two genes. They noted an excess of genetic variation being maintained in the region of glycophorin A that plays a critical role of entry of the malaria parasite into the blood cell.

“This signature of selection was strongest in populations that have the highest exposure to malaria,” Tishkoff said.

In addition, the researchers identified a novel protein variant at glycophorin B in several populations with high levels of malaria that may also be a target of natural selection.

Comparisons to chimpanzee and orangutan genomes showed that these mutations occurred after the human lineage split from these closely related primates. But a process known as “gene conversion,” in which similar genes can acquire mutations from one another during cell division, complicates tracking the exact history of the mutation’s spread.

“The genes for glycophorin A and B arose through gene duplication.  They are more than 95 percent similar to each other on the sequence level,” Ko said. “Because they are so similar, sequences of A might bind to B during recombination, which means a mutation that occurs on one can be shared with the other.”

That aspect of gene conversion may be a key to helping humans in the genetic arms race against malaria.

“The parasite’s genome is very highly mutable, and its generation time is short, as compared to humans, so having more mutations more quickly is helpful in keeping up,” Ko said. “This is one tool in the arms race. It may not win the war, but it’s another way to increase variation.”

A better understanding of the interplay between the genes of the malaria parasite and that of its human hosts could also give researchers an artificial advantage — drugs or vaccines — in the fight against the disease.

“Any new information about how malaria infects cells and how humans have evolved natural defense mechanisms against that infection adds to the body of knowledge about the pathology of malaria,” Tishkoff said. “This information could aid in the development of more effective treatments against malaria.”

In addition to Ko and Tishkoff, the research was conducted by Kristin A. Kaercher, Alessia Ranciaro and Jibril B. Hirbo of Penn; Emanuela Giombini and Paolo Marcatili of the Department of Biochemical Sciences at the University of Rome; Alain Froment of the Musee de l’ Homme, Paris: Muntaser Ibrahim of the Department of Molecular Biology and the Institute of Endemic Diseases at the University of Khartoum; Godfrey Lema and Thomas B. Nyambo of the Department of Biochemistry at the Muhimbili University of Health and Allied Sciences in Dar es Salaam, Tanzania; Sabah A. Omar of the Kenya Medical Research Institute; and Charles Wambebe of International Biomedical Research in Africa in Abuja, Nigeria.

Their research was supported by the Human Frontiers in Science Program, the National Science Foundation and the National Institutes of Health, and published online in the journal American Journal of Human Genetics today.

Source: Media Newswire