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Updated: Jun 8, 2026
A Rat Model of EcoHIV Brain Infection
Published on: January 21, 2021
TNFRSF11B computational development network construction and analysis between frontal cortex of HIV encephalitis
Ju X Huang1, L Wang1, Ming H Jiang2
1Biomedical Center, School of Electronics Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Background:
TNFRSF11B computational development network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy.
Methods:
By integration of gene regulatory network infer (GRNInfer) and the database for annotation, visualization and integrated discovery (DAVID) we identified and constructed significant molecule TNFRSF11B development network from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726.
Results:
Our result verified TNFRSF11B developmental process only in the downstream of frontal cortex of HIVE-control patients (BST2, DGKG, GAS1, PDCD4, TGFBR3, VEZF1 inhibition), whereas in the upstream of frontal cortex of HIVE (DGKG, PDCD4 activation) and downstream (CFDP1, DGKG, GAS1, PAX6 activation; BST2, PDCD4, TGFBR3, VEZF1 inhibition). Importantly, we datamined that TNFRSF11B development cluster of HIVE is involved in T-cell mediated immunity, cell projection organization and cell motion (only in HIVE terms) without apoptosis, plasma membrane and kinase activity (only in HIVE-control patients terms), the condition is vital to inflammation, brain morphology and cognition impairment of HIVE. Our result demonstrated that common terms in both HIVE-control patients and HIVE include developmental process, signal transduction, negative regulation of cell proliferation, RNA-binding, zinc-finger, cell development, positive regulation of biological process and cell differentiation.
Conclusions:
We deduced the stronger TNFRSF11B development network in HIVE consistent with our number computation. It would be necessary of the stronger TNFRSF11B development function to inflammation, brain morphology and cognition of HIVE.
