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Srivastava, B.

Publications and source records attributed to Srivastava, B..

2 recordsLinked to original sources

Genotyping of paired clinical isolates using PvCSP, PvMSP3α PvMSP3βand exploring STRs to differentiate between relapse and reinfection in P. vivax

The challenge of eliminating Vivax malaria is due to the relapses caused by hypnozoites. Despite several attempts to identify molecular markers to differentiate between relapse and new infection, a reliable marker has not yet been established. To address this issue, a genomic study was conducted on paired samples of patients who had experienced Plasmodium vivax infection twice. Genotyping was performed on paired samples from 10 vivax malaria patients using five molecular markers to distinguish between relapse and new infection. Our findings indicate that one sample represented a second episode that was a relapse of the first, while another sample had three episodes, two of which were relapse episodes. We combined our clinical records with molecular inferences to identify each pair as a relapse. This particular study provides a momentary view of forthcoming research endeavors that could be undertaken to distinguish between a relapse and a novel infection. Given the notable genetic variability of Plasmodium vivax, it is crucial to harness various markers to discern between relapse and new infection. The findings of this study are poised to be of immense utility for upcoming marker research in the aforesaid aspect.

genomics↗

Rab7 dependent regulation of goblet cell protein CLCA1 modulates gastrointestinal homeostasis

Inflammation in ulcerative colitis is typically restricted to the mucosal layer of distal gut. Disrupted mucus barrier coupled with microbial dysbiosis has been reported to occur prior to the onset of inflammation. Here, we show the involvement of vesicular trafficking protein Rab7 in regulating the colonic mucus system. We identified a lowered Rab7 expression in goblet cells of colon during human and murine colitis. In vivo Rab7 knocked down mice (Rab7KD) displayed a compromised mucus layer, increased microbial permeability and depleted gut microbiota with enhanced susceptibility to dextran sodium-sulfate induced colitis. These abnormalities emerged owing to altered mucus composition, as revealed by mucus proteomics, with increased expression of mucin protease Chloride channel accessory 1 (CLCA1). Mechanistically, Rab7 maintained optimal CLCA1 levels by controlling its lysosomal degradation, a process that was dysregulated during colitis. Overall, our work establishes a role for Rab7 dependent control of CLCA1 secretion required for maintaining mucosal homeostasis.

cell biology↗