Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I

N Engl J Med. 2006 Dec 28;355(26):2752-6. doi: 10.1056/NEJMoa063265.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Apolipoprotein L1
  • Apolipoproteins / deficiency*
  • Apolipoproteins / genetics*
  • Apolipoproteins / therapeutic use
  • Frameshift Mutation*
  • Humans
  • Lipoproteins, HDL / deficiency*
  • Lipoproteins, HDL / genetics*
  • Lipoproteins, HDL / therapeutic use
  • Male
  • Molecular Sequence Data
  • Recombinant Proteins / therapeutic use
  • Trypanosoma* / isolation & purification
  • Trypanosomiasis / drug therapy
  • Trypanosomiasis / genetics*


  • APOL1 protein, human
  • Apolipoprotein L1
  • Apolipoproteins
  • Lipoproteins, HDL
  • Recombinant Proteins