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malaria is back again, and this time with a trans-generational implication. According to a recent report, first pregnancies undo the relative resistance against _Plasmodium falciparum_ , the

most serious form of malarial parasite. The resistance seems to improve with subsequent pregnancies. The distinct clinical entity is known as maternal malaria. The symptoms associated with

this disease are premature delivery, intrauterine growth retardations, perinatal infant mortality, maternal anaemia, the infant being more prone to low birth weight and subsequent

susceptibility to disease and death. Till now, medical experts had blamed the immuno-compromised state of the expectant mother. But the fact that the disease gets less severe during

subsequent pregnancies shakes this belief. Research work of Michal Fried and Patrick Duffy at the us Army Medical Research Unit and the Kenya Medical Research Institute, both in Kisumu,

Kenya, has shown the occurrance of _P falciparum_ infected red blood cells (rbc) in the placenta of pregnant women, even when the parasite counts were statistically low in blood circulation.

The researchers say that the infected rbc bind to a particular protein receptor -- Chondroitin Sulphate a (csa) -- present in extracellular matrix of the placental tissues. The two have

reported the ability of infected rbc to bind to frozen samples of placental tissue, even from uninfected mothers. Furthermore, this binding pattern would be observed by adding csa protein to

the infected cells. Thus it was proved beyond doubt that csa did act as a receptor for parasite infected cells. It has also been noted previously that infected cells in general bind to a

protein called cd36, located on the surface of the endothelial cells. The blood circulation of infected pregnant women does contain a mixed population of cd36 and csa binding cells, but in

the case of non-pregnant women, the parasitised cells could bind only to cd36. These results suggest that the malarial parasite is able to exploit the oppurtunity presented by pregnancy, and

that the placental cells are a distinct subpopulation of cells with different cell surface binding proteins. The situation is finely balanced in favour of the parasite, because of a family

of parasite genes known as _var _ genes, with number of members ranging anywhere between 50-150 genes. By hiding out in placenta, the infected cells provide a persistant source of infection.

But the immune system gradually identifies these cells, and mounts a stronger response during subsequent pregnancies. The puzzle is not completely solved, however: csa is found fairly

well-distributed in all body tissues, so it is odd that the infected rbc bind to it only in the placenta. Duffy and Fried suggest that the cells and csa react most efficiently in placenta.

But nevertheless, armed with more information about the molecular interactions surface binding proteins, csa and genetics of _var _ family, researchers speculate a therapeutic course of

medication for maternal malaria, that blocks the infected cells' ability to bind to csa. The csa story is being hailed as "the first fresh idea on the problem we have had in

ages," says Louis Miller, chief of the Laboratory of Parasitic Diseases at the us National Institute ( _Science_ , Vol 272, No 5267).