Global distribution of a variant of the circumsporozoite gene of Plasmodium vivax

Article Abstract:

Malaria is a chronic disease caused by the infection of red blood cells with the parasite sporozoan Plasmodium, which is transmitted by mosquito bites or blood transfusion. The life cycle of Plasmodium can be divided into the asexual phase, which occurs in man, and the sexual phase, which occurs in the mosquito. The sporozoite form of Plasmodium enters man and invades tissue cells, such as liver cells. After 7 to 10 days, the sporozoites infect red blood cells and undergo schizogony, or several cell divisions, producing the merozoite form. The merozoites are released and invade other red blood cells, causing their destruction. This phase of the cycle is associated with symptoms of chills and fever. The merozoites are eventually transformed into microgametes or macrogametes, which are sucked up by the mosquito. The conventional treatment of malaria has proven inadequate, and efforts have focused on the development of a vaccine against the sporozoite stage of Plasmodium falciparum and Plasmodium vivax. The development of a vaccine for P. vivax is based on the presence of a surface protein on P. vivax sporozoites. However, recent studies have shown that the gene that codes for this surface protein varies in different forms of P. vivax. The DNA, or genetic material, of P. vivax was isolated and analyzed to determine the extent of variation in P. vivax forms from South America, the Indian subcontinent, and West Africa. Analyses showed that one genetic variant, or form that is slightly different from the predominant form, was detected in samples from all three geographic regions. In addition, five of six patients tested were shown to be infected by both the predominant and variant forms of P. vivax. These findings suggest that the development of a vaccine that is directed against a single component, such as the surface protein of P. vivax, may not be effective in controlling malaria. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Physiological aspects, Genetic aspects, Malaria vaccine, Malaria vaccines, Plasmodium, Plasmodium (Protozoa)

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Pentoxifylline prevents murine cerebral malaria

Article Abstract:

Nonimmune persons infected with Plasmodium falciparum are frequent victims of fatal cases of cerebral malaria (CM). Elevated levels of a substance released by the immune system known as tumor necrosis factor (TNF) have been observed in severe cases. TNF levels declined as the patient recovered. Since TNF is a mediator in the development of CM, the use of drugs inhibiting TNF production may have therapeutic value in CM control. The ability of pentoxifylline, a drug that inhibits excess TNF synthesis, to control CM was studied in an animal model. Genetically susceptible mice were divided into treatment and control groups, and then infected with Plasmodium berghei ANKA (PB). The treatment group received pentoxifylline for 10 consecutive days; the control group received inert saline. Survival times and clinical responses were noted. Neurologic signs were indicators of CM. Death occurred within five hours after the onset of neural symptoms. Control animals developed symptoms and died within 9 to 15 days after infection. None of the treated mice died within 21 days after infection. TNF bioactivity levels were elevated in control animals, and undetectable in pentoxifylline-treated animals. The mechanism of TNF action in the development of CM remains unclear. While pentoxifylline appears to prevent CM in susceptible mice, no impact on parasitemia (presence of the parasite in the blood) was observed. All animals had developed greater than 60 percent parasitemia at death within four to five weeks after infection, without evidence of neurological involvement. Pentoxifylline seems to have potential as supportive therapy in cases of falciparum malaria to prevent death from cerebral malaria. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Management, Evaluation, Tumor necrosis factor, Plasmodium falciparum, Pentoxifylline

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