Malaria: Evolutionary Biology

Malaria life cycle illustration.
National Institute of Allergy and Infectious Diseases

The malaria parasite is easily killed by electromagnetic frequencies and there are a number of small pilot projects using zappers in Africa. I’ve talked with some of the larger nonprofits about expanding these studies as I have seen 100% remission consistently with a few hours of application of exact frequencies. However, the response has been that if a non-profit research institute looked at anything other than conventional drugs they would get all their grants terminated.

It is important to keep up with the latest research on malaria as frequencies can also modify protein production. Virulent forms of this and other diseases (particular viral infections) can kill by evoking an overwhelming immune response. Thus frequencies must modulate immune response through reducing certain protein production as well as kill the pathogen. Those who are intelligent enough to use this technology can at least protect themselves.

Work on malaria frequencies at the recent Frequency Foundation workshop in San Diego has identified several new strains of the malaria parasite. These are available to subscribers as Malaria 2.0 frequencies.

Evolution of virulence in malaria
Bridget Penman email and Sunetra Gupta email
Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK
Journal of Biology 2008, 7:22doi:10.1186/jbiol83

The electronic version of this article is the complete one and can be found online at:
Published: 28 August 2008 © 2008 BioMed Central Ltd

The pathogenesis of severe malarial disease is not yet fully understood. It is clear that host immunopathology plays a central role, and a recent paper in BMC Evolutionary Biology suggests that the ability of the parasite to stimulate interleukin-10 production is a major factor and speculates on its impact on the coevolution of host and parasite.

Plasmodium falciparum malaria is responsible for over 1 million deaths each year, mostly in children under the age of 5 living in sub-Saharan Africa. And yet the number of malaria infections which go on to become life threatening is proportionally very small, as the majority of these infections either remain asymptomatic (due to the acquisition of clinical but non-sterile immunity after repeated exposure) or progress to disease without lethal complications [1]. Viewed in an evolutionary context, the existence of severe disease presents a population-level compromise for the parasite between the necessity of bearing factors that increase survival and transmission and the risk that these will stimulate a host immune response that will either curtail the infection or perversely cause the death of the host (thus also spelling the end for the parasite). With the aim of identifying factors that may be relevant in the evolution of this balance, Long et al. in a recent article in BMC Evolutionary Biology [2] have investigated the influence of the inflammatory response on the severity of disease in a rodent model of malaria, and we discuss here how their results may bear on the coevolution of parasite and host, in the context of what is known about the determinants of severe malarial disease in humans.
Factors in the severity of malaria

Severe malaria can be resolved broadly into two different syndromes: cerebral malaria and severe malarial anemia. Cerebral malaria is associated with impaired consciousness and sometimes convulsions and coma, and can leave those who recover with long-term neurological problems. Its pathophysiology is not fully understood but it is probably due to a combination of the obstruction of cerebral capillaries by parasitized cells and an overactive inflammatory response. Severe malarial anemia occurs when the suppression of erythrocyte production, combined with the destruction of red blood cells by the parasite itself, leads to a particularly profound anemia – which can cause shock and respiratory distress. Both syndromes can involve a range of metabolic complications such as acidosis or hypoglycemia [3].

Both host and parasite factors are likely to contribute to the processes leading to severe disease, and Long et al. have examined one possible interaction using mice infected with different clones of the rodent malaria parasite Plasmodium chabaudi chabaudi. Specifically, they have shown that blockade of the receptor for the anti-inflammatory cytokine interleukin-10 (IL-10) has a dramatic impact on time to death of the infected animal, particularly where the infecting parasite clones are normally avirulent. This result certainly implies that IL-10 plays a fundamental role in controlling the inflammatory response to malaria and that its absence can contribute to the demise of the murine host; Long et al. propose that the ability of the parasite to stimulate IL-10 production is a factor determining its relative virulence. However, whether regulation of the inflammatory response by IL-10 actually plays a part in the evolution of parasite virulence remains an open question and requires a careful consideration of the population-level consequences of interactions between host susceptibility and parasite virulence factors.

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