Background: Regulatory roles of long noncoding RNAs (lncRNAs) during viral infection has become more evident in last decade, but are yet to be explored for SARS-CoV-2. Materials & methods: We analy...

Background: Due to its rapid lethal effect in the early development stage of shrimp, acute hepatopancreatic necrosis disease (AHPND) has been causing great economic losses, since its first outbreak in southeast China in 2009. Vibrio parahaemolyticus, carrying the pirA and pirB toxin genes is known to cause AHPND in shrimp. The overall objective of this study was to sequence the whole genome of AHPND positive V. parahaemolyticus strains isolated from shrimp (Peneaus monodon) of the south-west region of Bangladesh in 2016 and 2017 and characterize the genomic features and emergence pattern of this marine pathogen. Results: Two targeted AHPND positive V. parahaemolyticus strains were confirmed using PCR with 16S rRNA, ldh, AP3 and AP4 primers. The assembled genomes of strain MSR16 and MSR17 were comprised of a total of 5,393,740 bp and 5,241,592 bp, respectively. From annotation, several virulence genes involved in chemotaxis and motility, EPS type II secretion system, Type III secretion system-1 (T3SS-1) and its secreted effectors, thermolabile hemolysin were found in both strains. Importantly, the ~ 69 kb plasmid was identified in both MSR16 and MSR17 strains containing the two toxin genes pirA and pirB. Antibiotic resistance genes were predicted against β-lactam, fluoroquinolone, tetracycline and macrolide groups in both MSR16 and MSR17 strains. Conclusions: The findings of this research may facilitate the tracking of pathogenic and/or antibiotic-resistant V. parahaemolyticus isolates between production sites, and the identification of candidate strains for the production of vaccines as an aid to control of this devastating disease. Also, the emergence pattern of this pathogen can be highlighted to determine the characteristic differences of other strains found all over the world.

Objective: Human Papillomavirus (HPV) is comprised of about 120 genotypic related viruses, classified into low- and high-risk HPVs, are capable of replicating inside the keratinocytes of skin or mucous membranes. Studies suggest that infections with HPV-16, HPV-18 have a higher rate of developing cancer. The aim of this study was to detect HPV early and estimate the genotype-specific prevalence of HPV in apparently healthy and asymptomatic females of Bangladesh. Method: After the cervical swab specimen collection, VIA test was performed to identify any type of abnormality in the cervix. A multiplex PCR amplification of HPV DNA using L1 consensus primer systems was done with type-specific primers followed by sequencing to detect HPV genotypes. Result: Amongst the 417 females, 121 were found to be HPV positive. The most prevalent high risk HPV genotypes were found to be HPV-16 and HPV-18. Different patient demographical parameters such as age, socioeconomic status, education, and history of first intercourse were also studied to find out the correlation with the HPV infection. Conclusion: Our results might provide some insights that influence on the development of cervical cancer. It also can help in better patient management, creating public health awareness, further testing, and implementation of existing vaccines.

Human natural killer (NK) cells can be sub-divided into two functional subsets but the clinical significance of these CD56^bright and CD56^dim NK cells in anti-tumour immunity remains largely unexplored. We determined the relative abundances of gene signatures for CD56^bright and CD56^dim NK cells along with 3 stromal and 18 other immune cell types in the patient tumour transcriptomes from the cancer genome atlas bladder cancer dataset (TCGA-BLCA). Using this computational approach, CD56^bright NK cells were predicted to be the more abundant tumour-infiltrating NK subset which was also associated with improved patient prognosis. A similar favorable survival trend was projected using gene signatures for mature myeloid dendritic cells (mDC) and CD8⁺ effector memory T cells (T_EM) and unveiled a potential CD56^bright NK-mDC-CD8⁺T cell crosstalk in the BLCA tumour microenvironment. Expression of transcripts encoding the activating NK cell receptors, NKG2D, NKp44, CD2, and CD160, showed positive survival trends in combination with CD56^bright NK cell infiltration. Transcription factors including HOBIT, IRF3, and STAT2 were also correlated with CD56^bright NK cell abundance. Additionally, a HOBIT-dependent tissue-residency program correlated with the CD56^bright NK and CD8⁺ T_EM cell signatures was found to be associated with favourable BLCA patient survival. Overall, our study highlights the significance of CD56^bright NK cells in BLCA patient prognosis. Our findings facilitate a better understanding of the NK cell anti-tumour responses that may ultimately lead to the development of promising NK and T cell-based therapies for BLCA.

Background: MicroRNAs are ~ 22-nucleotide-long biological modifiers that act as the post-transcriptional modulator of gene expression. Some of them are identified to be embedded within the introns of protein-coding genes, these miRNAs are called the intronic miRNAs. Previous findings state that these intronic miRNAs are co-expressed with their host genes. This co-expression is necessary to maintain the robustness of the biological system. Till to date, only a few experiments are performed discretely to elucidate the functional relationship between few co-expressed intronic miRNAs and their associated host genes. Results: In this study, we have interpreted the underlying modulatory mechanisms of intronic miRNA hsa-miR-933 on its target host gene ATF2 and found that aberration can lead to several disease conditions. A protein-protein interaction network-based approach was adopted, and functional enrichment analysis was performed to elucidate the significantly over-represented biological functions and pathways of the common targets. Our approach delineated that hsa-miR-933 might control the hyperglycemic condition and hyperinsulinism by regulating ATF2 target genes MAP4K4, PRKCE, PEA15, BDNF, PRKACB, and GNAS which can otherwise lead to the development of type II diabetes mellitus. Moreover, we showed that hsa-miR-933 can regulate a target of ATF2, brain-derived neurotrophic factor (BDNF), to modulate the optimal expression of ATF2 in neuron cells to render neuroprotection for the inhibition of neurodegenerative diseases. Conclusions: Our in silico model provides interesting resources for experimentations in a model organism or cell line for further validation. These findings may extend the common perception of gene expression analysis with new regulatory functionality.