Rapid Fire Presentation 8th International Conference on Plasmodium vivax Research 2022

Genetic profiling of drug resistance genes in Plasmodium vivax field isolates from Northern and Western regions of India. (#408)

Suman Tamang 1 , Karamveer Dr. Yadav 1 , Aditi Arya 1 , Amit Dr. Sharma 1 2 , Vineeta Dr. Singh 1
  1. Indian Council of Medical Research (ICMR) - National Institute of Malaria Research (NIMR), New Delhi, India., Dwarka, DELHI, India
  2. Molecular Medicine Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, Delhi, India

Introduction: Genetic profiling of molecular markers plays important role in identification and keep track of the prevalence of key mutations. Polymorphisms in P. vivax dhfr and dhps genes have been found to be associated with Sulfadoxine-Pyrimethamine (SP) resistance.  In country like India where Pv and Pf are almost equally prevalent, due to misdiagnosis and mixed infections cases, Pv getting exposed to SP is inevitable, so monitoring drug selective pressure and resistance is important to understand the therapeutic efficacy of SP in Pv. Unlike its ortholog (PfK13) from P. falciparum involvement of Pvk12 gene in artemisinin resistance has not been established yet, but it’s a potential candidate for investigation.  Our study was undertaken to access the genetic diversity of genes: Pvdhps, Pvdhfr and Pvk12 in Pv isolates from Northern and Western regions of India.

Methods: DBS collected from Delhi and Goa regions were analysed for aforesaid genes (Pvk12, Pvdhps and Pvdhfr) using PCR and sequenced to access their genetic profile.

Results: Of the 50 isolates analysed for Pvdhps gene, 13 isolates (26%) showed presence of A383G mutation, and novel mutation K512N was observed in three field isolates (6%). Sequence analysis of Pvdhfr gene revealed presence S58R mutation in seven isolates (23%) of 30 isolates analysed, as well as seven other isolates (23%) showed the S117N mutation. Out of 30 isolates, six (20%) showed novel K264R K12 mutation, remaining all isolates (80%) showed wild type Pvk12 genotype.

Conclusions: Presence of mutant genotypes for Pvdhfr and Pvdhps genes indicates emergence of resistance to SP drugs in Pv in these areas though the drug might be still effective. Our study suggests that research addressing therapeutic efficacy of SP in case of Pv should be carried out. Although, previously reported polymorphisms were not seen in Pvk12, it still remains a potential candidate for further investigations.