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Persistent pneumococcal colonisation in antiretroviral-treated HIV infection is associated with nasal inflammation

Joseph Aston Phiri1,2, Lusako Lucky Sibale3,4, Gloria Kapira3,4

  • 1Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi. jphiri@mlw.mw.

Nature Communications
|December 15, 2025
PubMed

Insights

Long-term antiretroviral therapy (ART) does not restore nasal immunity in people with HIV (PLHIV). Persistent inflammation and immune cell dysfunction contribute to pneumococcal carriage, suggesting new therapeutic targets.

Area of Science:

  • Immunology
  • Infectious Diseases
  • HIV Research

Background:

  • People living with HIV (PLHIV) on antiretroviral therapy (ART) experience increased susceptibility to pneumococcal infections.
  • Systemic viral suppression via ART does not fully restore mucosal immunity in the respiratory tract.

Purpose of the Study:

  • To investigate the persistent effects of long-term ART on nasal mucosal immunity in PLHIV.
  • To identify immune signatures associated with increased susceptibility to pneumococcal colonization in PLHIV on ART.

Main Methods:

  • Flow cytometry and single-cell transcriptomics were used to analyze nasal immune cells.
  • Neutrophil functional assays were performed to assess oxidative burst capacity.
  • Gene expression analysis identified epithelial and T cell profiles and senescence-associated secretory phenotype (SASP).

Main Results:

  • Long-term ART (over 1 year) did not restore nasal mucosal immunity in PLHIV.
  • A persistent immune signature was observed, characterized by epithelial-driven neutrophilic inflammation, T cell exhaustion, and cellular senescence.
  • Neutrophils showed mitochondrial stress, SASP gene expression, and impaired function, especially in those with pneumococcal carriage.
  • Epithelial cells upregulated neutrophil-recruiting ligands, and nasal T cells exhibited pro-apoptotic and exhaustion profiles.
  • Neutrophilic inflammation correlated with pneumococcal carriage density, suggesting a feedback loop.

Conclusions:

  • Tissue-specific immune dysregulation persists in PLHIV despite ART.
  • Targeting epithelial-immune signaling or neutrophil senescence may offer novel strategies to reduce respiratory pathogen burden in PLHIV.

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