Format

Send to

Choose Destination
Elife. 2016 Mar 22;5. pii: e12613. doi: 10.7554/eLife.12613.

Evolutionary genomics of epidemic visceral leishmaniasis in the Indian subcontinent.

Author information

1
Department of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
2
Wellcome Trust Sanger Institute, Hinxton, United Kingdom.
3
School of Maths, Applied Maths and Statistics, National University of Ireland Galway, Galway, Ireland.
4
BP Koirala Institute of Health Sciences, Dharan, Nepal.
5
Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
6
Telethon Kids Institute, University of Western Australia, Perth, Australia.
7
Institut für Mikrobiologie und Hygiene, Charité Universitätsmedizin Berlin, Berlin, Germany.
8
Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
9
Department of Chemistry and Chemical Biology, Northeastern University, Boston, United States.
10
Laboratory of Molecular Parasitology, Université Libre de Bruxelles, Gosselies, Belgium.
11
Department of Infectious Diseases and Immunology, Council of Scientific and Industrial Research, Indian Institute of Chemical Biology, Kolkata, India.
12
Department of Public Health, Institute of Tropical Medicine, Antwerp, Belgium.
13
Department of Biomedical Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Antwerp, Belgium.

Abstract

Leishmania donovani causes visceral leishmaniasis (VL), the second most deadly vector-borne parasitic disease. A recent epidemic in the Indian subcontinent (ISC) caused up to 80% of global VL and over 30,000 deaths per year. Resistance against antimonial drugs has probably been a contributing factor in the persistence of this epidemic. Here we use whole genome sequences from 204 clinical isolates to track the evolution and epidemiology of L. donovani from the ISC. We identify independent radiations that have emerged since a bottleneck coincident with 1960s DDT spraying campaigns. A genetically distinct population frequently resistant to antimonials has a two base-pair insertion in the aquaglyceroporin gene LdAQP1 that prevents the transport of trivalent antimonials. We find evidence of genetic exchange between ISC populations, and show that the mutation in LdAQP1 has spread by recombination. Our results reveal the complexity of L. donovani evolution in the ISC in response to drug treatment.

KEYWORDS:

epidemiology; evolution; genomics; global health; infectious disease; leishmania donovani; microbiology

PMID:
27003289
PMCID:
PMC4811772
DOI:
10.7554/eLife.12613
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for eLife Sciences Publications, Ltd Icon for PubMed Central
Loading ...
Support Center