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Black fever parasite beats drugs by adding just two DNA bases to its genome

Reporter: Aviva Lev-Ari, PhD, RN

 

 

 

 

 

Wellcome Trust Sanger Institute scientists show how the parasite responsible for the neglected tropical disease Black Fever (visceral leishmaniasis) can become immune to drug treatment. Studying the whole genomes of more than 200 samples of Leishmania donovani revealed that the addition of just two bases of DNA to a gene known as LdAQP1 stops the parasite from absorbing antimonial drugs.

While antimonials are no longer the first-line treatment for the disease, the discovery does show that whole-genome sequencing of L. donovani parasites could be used to study and track the emergence of resistance to frontline drugs – alerting health workers to potential hot spots of resistance.

Black Fever is the second most deadly parasitic disease after malaria, affecting nearly 300,000 people every year and killing up to 50,000. The parasite is mainly found in the Indian subcontinent, where up to 80 per cent of the disease occurs. To best understand how the parasite evolves and track the spread of drug resistance, researchers need a way to survey and monitor the parasite’s population structure. Unfortunately standard techniques to do this have proved fruitless because the strains of L. donovani parasite are so genetically similar.

Exploring the genetic landscape of L. donovani at such depth and breadth yielded new insights into the parasites’ ability to develop drug resistance, and its evolutionary history. In particular, the researchers found that the insertion of just two bases of DNA into the genome of approximately 35,000,000 bases helped the parasite to overcome antimonial drugs.

Sourced through Scoop.it from: www.sanger.ac.uk

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