• DEEPTI DEOBAGKAR

      Articles written in Journal of Biosciences

    • White Spot Syndrome Virus infection in Penaeus monodon is facilitated by housekeeping molecules

      Vinayak Biradar Santosh Narwade Mandar Paingankar Deepti Deobagkar

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      White Spot Syndrome Virus (WSSV) is a major pathogen in shrimp aquaculture, and its rampant spread has resulted in great economic loss. Identification of host cellular proteins interacting with WSSV will help in unravelling the repertoire of host proteins involved in WSSV infection. In this study, we have employed one-dimensional and two-dimension virus overlay protein binding assay (VOPBA) followed by matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) to identify the host proteins of Penaeus monodon that could interact with WSSV. The VOPBA results suggest that WSSV interacted with housekeeping proteins such as heat shock protein 70, ATP synthase subunit 𝛽, phosphopyruvate hydratase, allergen Pen m 2, glyceraldehyde-3-phosphate dehydrogenase, sarcoplasmic calcium-binding protein, actin and 14-3-3-like protein. Our findings suggest that WSSV exploits an array of housekeeping proteins for its transmission and propagation in P. monodon.

    • Analysis of drug resistance marker genes of Plasmodium falciparum after implementation of artemisinin-based combination therapy in Pune district, India

      AARTI OZARKAR ABHISHEK KANYAL SWATI DASS PRAKASH DESHPANDE DEEPTI DEOBAGKAR KRISHANPAL KARMODIYA

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      The global emergence and spread of malaria parasites resistant to antimalarial drugs is a major problem inmalaria control and elimination. In this study, samples from Pune district were characterized to determineprevalence of molecular markers of resistance to chloroquine (pfcrt codons C72S, M74I, N75E, K76T andpfmdr-1 N86Y, Y184F), pyrimethamine (pfdhfr C50R, N51I, C59R, S108N), sulfadoxine (pfdhps, S436A,A437G, K540E, A581G), and artemisinin (pfkelch13, C580Y, R539T). The pfcrt K76T mutation was found in78% samples as CVMNT, SVMNT and CVIET haplotype. The pfmdr-1 N86Y and Y184F mutations werefound in 54% of samples. The pfdhfr double mutation C59R + S108N was present in 67% of samples, whilethe pfdhfr triple mutation (N51I + C59R + S108N) was not detected. The pfdhps mutations A437G andK540E were found in 67% of samples. Single mutants of pfdhps were rare, with K540E detected in only 6patient samples. Similarly, pfdhps A581G was found in 13 of the isolates. The molecular markers associatedwith artemisinin resistance (mutations in pfkelch13 C580Y, R539T) were not detected in any of the isolates.These results suggest an emerging problem with multidrug-resistant P. falciparum. Though the genotypeconventionally associated with artemisinin resistance was not observed, chloroquine-resistant genotype hasreached complete fixation in the population. Moreover, the prevalence of mutations in both pfdhfr and pfdhps,with the presence of the quadruple mutant, indicates that continued monitoring is required to assess whethersulfadoxine-pyrimethamine can be used efficiently as a partner drug for artemisinin for the treatment of P.falciparum.

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