ArticlePLoS pathogens2022
CD169-mediated restrictive SARS-CoV-2 infection of macrophages induces pro-inflammatory responses.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 48 citations in OpenAlex.
- Gapmers targeting conserved SARS-CoV-2 single-stranded regions reduce viral load and reshape inflammatory macrophage responses.iScience · 2026Article
- SARS-CoV-2 nucleocapsid induces hyperinflammation and vascular leakage through the Toll-like receptor signaling axis in macrophages.Science advances · 2026Article
- Genetic and transcriptomic determinants of disseminated coccidioidomycosis identify a founder variant inmedRxiv : the preprint server for health sciences · 2026Article
- Respiratory syncytial virus-induced SIGLEC1 upregulation inhibits macrophage autophagy and facilitates inflammatory mediator secretion.BMJ open respiratory research · 2026Article
- Review
- Role of myeloid cells expressing CD169/Siglec-1 in host-pathogen interactions.FEMS microbiology reviews · 2026Review
- Siglecs: From Biomodulation to Immunotherapy.Current protein & peptide science · 2026Review
- CD169-positive macrophages in lymph nodes and the tumor microenvironment: harnessing their biology for clinical diagnosis and anticancer therapeutic strategies.Frontiers in immunology · 2026Review
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Immunological and pathological roles of Siglecs: a molecular review.Frontiers in immunology · 2026Review
- CD169Frontiers in cellular and infection microbiology · 2026Article
- Hidden in Plain Sight: Alphavirus Persistence and Its Potential for Driving Chronic Pathogenesis.Viruses · 2025Review
- Deleterious variants in the autophagy-related gene RB1CC1/FIP200 impair immunity to SARS-CoV-2.Nature communications · 2025Article
- Incorporation of 5-methylcytidine alleviates RIG-I-mediated innate immune responses to a self-amplifying RNA vaccine.Science translational medicine · 2025Article
- Type I IFNs Decrease SARS-CoV-2 Replication in Human Cardiomyocytes and Increase Cytokine Production in Macrophages.Journal of clinical immunology · 2025Article
- Primary leptomeningeal histiocytic lymphoproliferative disorder associated with SARS-CoV-2 brain infection in k18-hACE2 mouse: a case report.Laboratory animal research · 2025Article
- Expression of intron-containing HIV-1 RNA induces NLRP1 inflammasome activation in myeloid cells.PLoS biology · 2025Article
- SARS-CoV-2 encoded ORF3a interacts with YY1 to promote latent HCMV reactivation.PLoS pathogens · 2025Article
- Toll-like receptor 7 (TLR7)-mediated antiviral response protects mice from lethal SARS-CoV-2 infection.Journal of virology · 2025Article
- A live attenuated SARS-CoV-2 vaccine constructed by dual inactivation of NSP16 and ORF3a.EBioMedicine · 2025Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Exacerbated and persistent innate immune response marked by pro-inflammatory cytokine expression is thought to be a major driver of chronic COVID-19 pathology. Although macrophages are not the primary target cells of SARS-CoV-2 infection in humans, viral RNA and antigens in activated monocytes and macrophages have been detected in post-mortem samples, and dysfunctional monocytes and macrophages have been hypothesized to contribute to a protracted hyper-inflammatory state in COVID-19 patients. In this study, we demonstrate that CD169, a myeloid cell specific I-type lectin, facilitated ACE2-independent SARS-CoV-2 fusion and entry in macrophages. CD169-mediated SARS-CoV-2 entry in macrophages resulted in expression of viral genomic and subgenomic RNAs with minimal viral protein expression and no infectious viral particle release, suggesting a post-entry restriction of the SARS-CoV-2 replication cycle. Intriguingly this post-entry replication block was alleviated by exogenous ACE2 expression in macrophages. Restricted expression of viral genomic and subgenomic RNA in CD169+ macrophages elicited a pro-inflammatory cytokine expression (TNFα, IL-6 and IL-1β) in a RIG-I, MDA-5 and MAVS-dependent manner, which was suppressed by remdesivir treatment. These findings suggest that de novo expression of SARS-CoV-2 RNA in macrophages contributes to the pro-inflammatory cytokine signature and that blocking CD169-mediated ACE2 independent infection and subsequent activation of macrophages by viral RNA might alleviate COVID-19-associated hyperinflammatory response.
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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.