Schistosomiasis: The mouse that wasn't immune

Article Abstract:

Individuals can develop immunity to schistosomiasis, an parasitic infection by the blood fluke, Schistosoma. The mechanisms for immunity are not completely understood, but much has been learned about the development of immunity using the mouse as an animal model. The parasites penetrate the skin as larvae, which are present in contaminated water, and travel through the blood stream to the heart, lungs, gastrointestinal tract, and liver, where they become adult schistosomula. The parasite can block blood vessels and cause cysts (areas of inflammation and infection) and scar tissues in many organs of the body, such as the liver, brain, and lung. Antibodies are produced against the antigens of the schistosomula and an immune response occurs, known as antibody-dependent cell-mediated cytotoxicity, that kills the parasite. In mice of strain 129, the parasite develops to the adult stage, but the worms are killed three to four weeks after infection. It is now known that the loss of infection is not due to differences in the ability of the mice to mount an immune response, but because of variations in the architecture of the blood vessels of the lungs and liver. In other mice, the worms migrate to the liver, but in the 129 strain, the worms lodge in the lungs and cannot get back to the liver. A strong antibody-dependent cell-mediated cytotoxic response occurs in the lungs that kills the parasite. In some infected 129 strain mice, connections of blood vessels have been observed between the liver and the lungs. In animals where the life cycle of the parasite cannot be completed, and infection cannot occur, the system of blood vessels in the liver and the lungs is shortened. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Blood vessels, Anatomy, Immune system, Cellular immunity, Schistosomiasis

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Variation and vaccination

Article Abstract:

The subject of genetic variation in the parasitic strains that cause malaria was discussed at a recent meeting in the Netherlands. Plasmodium falciparum, in particular, can now be analyzed with methods of molecular biology, immunology, and biochemistry; considerable variation even within a single infection are known to occur. This diversity results from different alleles at several loci; mutation (particularly when presented with antimalarial drugs); expression of different genes at different stages of the parasite's life-cycle; and the absence of genes as a result of chromosomal deletion. The genetic bases for resistance of malaria to the two most commonly used agents, chloroquine and pyrimethamine, are generally well understood, especially for the latter drug. The genes that encode key parasite proteins have been found to vary to a surprising extent: in one village in the Sudan, 29 isolates (parasite specimens) all had different genomes. This kind of variability differs from region to region; infections in Africa and South America tend to be mixed, but infections in Sri Lanka tend to be caused by organisms of a single clone. How parasite variants arise and how they are maintained still requires more research. Some theories favor random drift, some, selection pressure. Regardless of the cause, developing drugs for such protean agents is difficult. Sequences that appear stable, or that are present in all stages of the life-cycle, could be used as the basis for vaccines. The meeting also focused on the discouraging lack of new drugs to fight malaria; even the most recently introduced drug, mefloquine, is already associated with resistance. (Consumer Summary produced by Reliance Medical Information, Inc.)

Conferences, meetings and seminars, Product development, Drug therapy, Genetic aspects, Drug resistance in microorganisms, Microbial drug resistance, Malaria

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Another route to a vaccine?

Article Abstract:

A vaccine for malaria that disrupts the second or pre-erythrocytic phase of the parasite's life-cycle has become feasible. Adrian V.S. Hill and coworkers found that 1s6, a 9-amino-acid epitope derived from the liver-stage antigen LSA-1, can prevent the infection of hepatocytes or liver cells in this phase by binding to the HLA-B53 antigen molecule. This immunological approach may prove more effective than earlier vaccines that attacked the parasites in their initial or sporozoite phase.

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