A World Without Malaria

Malaria kills hundreds of thousands every year and infects millions more. Yet, elimination of the disease is possible. In fact, it’s been achieved in 62 countries since 1960. So what stands in the way of a world without malaria? Read more…

Blog Posts

2015 Malaria Resistance Issue

UC Davis collaborator Abou with children in Sidarebougou. Image courtesy of the Vector Genetics Lab at UC Davis.

Not So “Useless” Hybrids: The Emergence of Genetic Resistance to Insecticides in Anopheles Mosquitoes

People always gripe about how scientists waste time studying useless, obscure topics. I’ve spent my career studying the species Anopheles gambiae, whose name literally means “useless” in Greek. But it also happens to be the deadliest animal in the world: its other name is the African malaria mosquito. It may be a useless pest, but understanding it is critical to fighting malaria.

Malaria - Mekong

A Microbial Melting Pot – The Mekong Region and Antimalarial Resistance

The malaria parasite – and in particular, Plasmodium falciparum, the most deadly species – has been able to evolve resistance to several medications frequently used to treat the disease. While strains resistant to one form of treatment or another are now widespread, scientists have noted that the Mekong Region has frequently been the source of these new, drug-resistant strains.


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Targeting the Cell Stress Response of Plasmodium Falciparum to Overcome Artemisinin Resistance

Successful control of falciparum malaria depends greatly on treatment with artemisinin combination therapies. Thus, reports that resistance to artemisinins (ARTs) has emerged, and that the prevalence of this resistance is increasing, are alarming. The researchers’ model predicts that extending current three-day ART treatment courses to four days, or splitting the doses, will efficiently clear resistant parasite infections.

Challenges in Modelling Infectious DIsease Dynamics

Malaria, HIV, and tuberculosis (TB) collectively account for several million deaths each year, with all three ranking among the top ten killers in low-income countries. Despite being caused by very different organisms, malaria, HIV, and TB present a suite of challenges for mathematical modellers that are particularly pronounced in these infections, but represent general problems in infectious disease modelling, and highlight many of the challenges described throughout this issue. Here, we describe some of the unifying challenges that arise in modelling malaria, HIV, and TB, including variation in dynamics within the host, diversity in the pathogen, and heterogeneity in human contact networks and behaviour. Through the lens of these three pathogens, we provide specific examples of the other challenges in this issue and discuss their implications for informing public health efforts.

Landscape Ecology and Epidemiology of Malaria Associated with Rubber Plantations in Thailand: Integrated Approaches to Malaria Ecotoping

The agricultural land use changes that are human-induced changes in agroforestry ecosystems and in physical environmental conditions contribute substantially to the potential risks for malaria transmission in receptive areas. Due to the pattern and extent of land use change, the risks or negatively ecosystemic outcomes are the results of the dynamics of malaria transmission, the susceptibility of human populations, and the geographical distribution of malaria vectors. This review focused basically on what are the potential effects of agricultural land use change as a result of the expansion of rubber plantations in Thailand and how significant the ecotopes of malaria-associated rubber plantations (MRP) are.

A molecular mechanism of artemisinin resistance in Plasmodium falciparum malaria : Nature : Nature Publishing Group

Artemisinins are the cornerstone of anti-malarial drugs. Emergence and spread of resistance to them raises risk of wiping out recent gains achieved in reducing worldwide malaria burden and threatens future malaria control and elimination on a global level. Genome-wide association studies (GWAS) have revealed parasite genetic loci associated with artemisinin resistance. However, there is no consensus on biochemical targets of artemisinin. Whether and how these targets interact with genes identified by GWAS, remains unknown. Here we provide biochemical and cellular evidence that artemisinins are potent inhibitors of Plasmodium falciparum phosphatidylinositol-3-kinase (PfPI3K), revealing an unexpected mechanism of action.

Genetic Investigation of Tricarboxylic Acid Metabolism during the Plasmodium falciparum Life Cycle

New antimalarial drugs are urgently needed to control drug-resistant forms of the malaria parasite Plasmodium falciparum. Mitochondrial electron transport is the target of both existing and new antimalarials. Herein, we describe 11 genetic knockout (KO) lines that delete six of the eight mitochondrial tricarboxylic acid (TCA) cycle enzymes. Although all TCA KOs grew normally in asexual blood stages, these metabolic deficiencies halted life-cycle progression in later stages. Specifically, aconitase KO parasites arrested as late gametocytes, whereas α-ketoglutarate-dehydrogenase-deficient parasites failed to develop oocysts in the mosquitoes. Mass spectrometry analysis of 13C-isotope-labeled TCA mutant parasites showed that P. falciparum has significant flexibility in TCA metabolism. This flexibility manifested itself through changes in pathway fluxes and through altered exchange of substrates between cytosolic and mitochondrial pools. Our findings suggest that mitochondrial metabolic plasticity is essential for parasite development.

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