APOL1 null alleles from a rural village in India do not correlate with glomerulosclerosis.

Background: Among African-Americans, genome wide association revealed a strong correlation between the G1 and G2 alleles of APOL1 (apolipoproteinL1, also called trypanolytic factor) and kidney diseases including focal and segmental glomerulosclerosis, HIV-associated nephropathy and hypertensive nephrosclerosis. In the prevailing hypothesis, heterozygous APOL1 G1 and G2 alleles increase resistance against Trypanosoma that cause African sleeping sickness, resulting in positive selection of these alleles, but when homozygous the G1 and G2 alleles predispose to glomerulosclerosis. While efforts are underway to screen patients for G1 and G2 alleles and to better understand "APOL1 glomerulopathy," no data prove that these APOL1 sequence variants cause glomerulosclerosis.

Short report: Human trypanosomiasis caused by Trypanosoma evansi in a village in India: preliminary serologic survey of the local population.

After discovery of the first recorded case of human infection with Trypanosoma evansi, serologic screening of 1,806 persons from the village of origin of the patient in India was performed using the card agglutination test for trypanosomiasis and T. evansi. A total of 410 (22.

Human trypanosomiasis caused by Trypanosoma evansi in India: the first case report.

We report an Indian farmer who had fluctuating trypanosome parasitemia associated with febrile episodes for five months. Morphologic examination of the parasites indicated the presence of large numbers of trypanosomes belonging to the species Trypanosoma evansi, which is normally a causative agent of animal trypanosomiasis known as surra. Basic clinical and biologic examinations are described, using several assays, including parasitologic, serologic, and molecular biologic tests, all of which confirmed the infecting species as T.