Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I.
Humans have innate immunity against Trypanosoma brucei brucei that is known to involve apolipoprotein L-I (APOL1). Recently, a case of T. evansi infection in a human was identified in India. We investigated whether the APOL1 pathway was involved in this occurrence. The serum of the infected patient was found to have no trypanolytic activity, and the finding was linked to the lack of APOL1, which was due to frameshift mutations in both APOL1 alleles. Trypanolytic activity was restored by the addition of recombinant APOL1. The lack of APOL1 explained the patient's infection with T. evansi.
Vanhollebeke
Benoit
B
Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires, Université Libre de Bruxelles, Gosselies, Belgium.
Truc
Philippe
P
Poelvoorde
Philippe
P
Pays
Annette
A
Joshi
Prashant P
PP
Katti
Ravindra
R
Jannin
Jean G
JG
Pays
Etienne
E
D000595:Amino Acid Sequence; D000818:Animals; D000075944:Apolipoprotein L1; D001053:Apolipoproteins / Q000172:deficiency* / Q000235:genetics* / Q000627:therapeutic use; D016368:Frameshift Mutation; D006801:Humans; D008075:Lipoproteins, HDL / Q000172:deficiency* / Q000235:genetics* / Q000627:therapeutic use; D008297:Male; D008969:Molecular Sequence Data; D011994:Recombinant Proteins / Q000627:therapeutic use; D014345:Trypanosoma / Q000302:isolation & purification; D014352:Trypanosomiasis / Q000188:drug therapy / Q000235:genetics*
C108666:APOL1 protein, human; D000075944:Apolipoprotein L1; D001053:Apolipoproteins; D008075:Lipoproteins, HDL; D011994:Recombinant Proteins