ArticleCell discovery2021
Distinct uptake, amplification, and release of SARS-CoV-2 by M1 and M2 alveolar macrophages.
Article in Cell discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mucosal immune response in biology, disease prevention and treatment.Signal transduction and targeted therapy · 2025Pooled it
- Gapmers targeting conserved SARS-CoV-2 single-stranded regions reduce viral load and reshape inflammatory macrophage responses.iScience · 2026Article
- Fibrin-rich environment drives catheter-associated UTIs by suppressing macrophage defenses.Nature communications · 2026Article
- Real-Time Scanning Ion Conductance Microscopy Reveals MARCKS-Driven Morphological Remodeling and Nanomechanical Softening during LPS-Induced Macrophage Polarization.Analytical chemistry · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Combating respiratory diseases with mucosal vaccines.Journal of virology · 2026Review
- The macrophage entry mechanism of SARS-CoV-2 mediated by surface CD98/TMPRSS11E complex is associated with the cellular tropism toward proinflammatory M1 and pathogenesis.Respiratory research · 2026Article
- GM-CSF and M-CSF Driven Differentiation Differentially Regulates Chikungunya Virus Infection and Antiviral Responses in Human Monocyte-Derived Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Dynamic metabolic modelling of ATP allocation during viral infection.Journal of the Royal Society, Interface · 2026Article
- SARS-CoV-2-International journal of microbiology · 2026Review
- Respiratory epithelial cells as central mediators of immune crosstalk in SARS-CoV-2 infection.Frontiers in immunology · 2026Review
- Article
- Understanding of endo/lysosomal escape of nanomaterials in biomedical application.Smart molecules : open access · 2025Review
- Investigating alveolar macrophages in an human ex vivo precision-cut lung slice model of SARS-CoV-2 infection using Raman spectroscopy-A case study.Clinical and translational medicine · 2025Article
- Human Alveolar Macrophages Detect SARS-CoV-2 Envelope Protein Through TLR2 and TLR4 and Secrete Cytokines in Response.Immunology · 2025Article
- Unraveling the cross-talk between a highly virulent PEDV strain and the host via single-cell transcriptomic analysis.Journal of virology · 2025Article
- Dexamethasone disrupts intracellular pH homeostasis to delay coronavirus infectious bronchitis virus cell entry via sodium hydrogen exchanger 3 activation.Journal of virology · 2025Article
- Article
- Monitoring Macrophage Polarization in Infectious Disease, Lesson From SARS-CoV-2 Infection.Reviews in medical virology · 2025Review
- Isolation and characterization of a protective monoclonal antibody targeting outer membrane protein (OmpA) against tuberculosis.Microbiology spectrum · 2025Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invades the alveoli, where abundant alveolar macrophages (AMs) reside. How AMs respond to SARS-CoV-2 invasion remains elusive. Here, we show that classically activated M1 AMs facilitate viral spread; however, alternatively activated M2 AMs limit the spread. M1 AMs utilize cellular softness to efficiently take up SARS-CoV-2. Subsequently, the invaded viruses take over the endo-lysosomal system to escape. M1 AMs have a lower endosomal pH, favoring membrane fusion and allowing the entry of viral RNA from the endosomes into the cytoplasm, where the virus achieves replication and is packaged to be released. In contrast, M2 AMs have a higher endosomal pH but a lower lysosomal pH, thus delivering the virus to lysosomes for degradation. In hACE2 transgenic mouse model, M1 AMs are found to facilitate SARS-CoV-2 infection of the lungs. These findings provide insights into the complex roles of AMs during SARS-CoV-2 infection, along with potential therapeutic targets.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.