The abstract is read at the publisher; the summary is JClub's.
HIV-1-infected C20 microglia show a graded, infection-level continuum in transcription and miRNA reprogramming, with interferon-α/β and EMT/hypoxia peaking at low infection and mTORC1/MYC rising at high infection.
- Why it matters: Antiviral therapy does not fully stop HIV-1–driven neuroinflammation because microglia can express viral products, but how productive replication level reshapes host programs is unclear.
- What they did: Single-cell RNA-seq of HIV-1-infected C20 microglia was stratified by HIV-1 splice junction-supporting reads into low- and high-infection groups, and differentially expressed miRNAs and genes were integrated using an inverse miRNA–target filter.
- The result: Immune and cell-cycle pathways were induced across infection levels, while interferon-α/β and EMT/hypoxia reversed with increasing viral burden; miRNA/mRNA networks included miR-33a-5p, miR-3065-3p, miR-107, and let-7c-5p, supporting candidate miRNA-mediated mechanisms.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.