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Biology subjects

Begum, M. N.

Publications and source records attributed to Begum, M. N..

2 recordsLinked to original sources

Genomic Surveillance of Respiratory Syncytial Virus among Patients with Acute Respiratory Infection through Hospital-Based Influenza Surveillance Platforms in Bangladesh, August 2024-December 2025

BackgroundRSV is one of the major contributing factors of acute lower respiratory tract infection among younger children who are below five years old; over 95% of the burden falls on low- and middle-income countries. Bangladesh faces a substantial pediatric RSV burden yet lacks post-pandemic whole-genome data. Approval of nirsevimab and maternal vaccines (Arexvy, Abrysvo), underscores the need for region-specific genomic surveillance to inform prevention and control strategies. ObjectivesTo conduct the whole-genome sequencing (WGS) study of RSV in Bangladeshi population, characterizing viral genotypic diversity, phylogenetics, F and G protein mutations, glycosylation dynamics, while generating and depositing complete genomes in GISAID. MethodsBetween August 2024 and December 2025, of 1,390 RSV-positive specimens (Ct [≤]35), 59 high-viral-load samples (Ct [≤]25) were selected for whole-genome sequencing using Oxford Nanopore Technology (ARTIC primers), assembled with MIRA v2.0.0, and analyzed via Augur/Nextstrain, Nextclade, and NetNGlyc/NetOGlyc 4.0. ResultsOf 11,874 patients, 1,390 (11.7%) were RSV-positive (RSV-A 94.6%). From selected 59 RSV-positive cases, 49 high-quality genomes were generated (83.1% pass; 94.7% completeness; median depth 1,500x, range 443-4,948): 43 RSV-A (ON1; A.D.3.7 63%, A.D.3 19%, A.D.3.12 9%, A.D.3.1 7%, A.D.1.11 2%) and 6 RSV-B (BA9/B.D.E.1). S276N at antigenic site II (34.9% RSV-A) and S389P in all RSV-B were detected; neither confers resistance to nirsevimab or palivizumab. An F protein N75 N-glycosylation site was fixed in all RSV-A; RSV-B acquired HVR2 N256 glycan in 67%. All 49 genomes were deposited in GISAID. ConclusionThis WGS study of RSV in the Bangladeshi population confirms LMIC nanopore surveillance feasibility, multi-lineage co-circulation, and intact conservation of all vaccine and antibody targets. Progressive glycan remodeling warrants monitoring. These findings establish a genomic baseline to guide nirsevimab and maternal vaccine deployment in Bangladesh, with direct relevance for RSV surveillance programs across South Asia.

evolutionary biology↗

Molecular Investigation of TSHR gene in Bangladeshi Congenital Hypothyroid patients

The disorder of thyroid gland development or thyroid dysgenesis (TH) accounts for 80-85% cases of congenital hypothyroidism (CH). Hence, the understanding of molecular etiology of TH is prerequisite. Mutations in TSHR gene is mostly associated with thyroid dysgenesis, prevent or disrupt normal development of the gland. The current study detects two nonsynonymous mutations (p.Ser508Leu, p.Asp727Glu) in transmembrane (TM)-region (Exon 10) of TSHR gene in 21 patients with dysgenesis by sequencing-based analysis. Later, transmembrane (TM)-region of TSHR protein is modelled by homology modeling. Transmembrane (TM)-region of TSHR protein is targeted by small molecules thyrogenic drugs, MS437 and MS438 to perceive the effect of mutations. The damaging effect in drug-protein complexes of mutants were envisaged by molecular docking and interactions. The binding affinity of wild type protein was much higher than the mutant cases for both of the ligands (MS437 and MS438). Molecular dynamics simulates dynamic behavior of wild type and mutant complexes. MS437-TSHR368-764MT2 and MS438-TSHR368-764MT1 show stable conformations in biological environments. Finally, PCA reveals structural and energy profile discrepancies. TSHR368-764MT1 exhibits much variations than TSHR368-764WT and TSHR368-764MT2, emphasizing more damaging pattern in TSHR368-764MT1. The study might be helpful to understand molecular etiology of thyroid dysgenesis (TH) exploring the mutational impact on TSHR protein to the interaction with agonists.

genetics↗