ArticleProceedings of the National Academy of Sciences of the United States of America2023
Riding apoptotic bodies for cell-cell transmission by African swine fever virus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 77 citations in OpenAlex.
- Article
- Single-cell spatial immune landscape of ASFV-infected porcine lung microenvironment.Virulence · 2026Article
- Distinct cytotoxic cell subsets underlie protective and non-protective immunity to African swine fever virus.Emerging microbes & infections · 2026Article
- FAM134B Restricts African Swine Fever Virus Capsid Assembly via Reticulophagy and Its Antiviral Activity is Antagonized by the Viral Virulence-Associated Factor pMGF300-2R.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuronal Apoptotic Bodies Facilitate Japanese Encephalitis Virus Infection and Pathogenicity.Journal of extracellular vesicles · 2026Article
- Correlates of protection against African swine fever virus identified by a systems immunology approach.eLife · 2026Article
- RPSA enhances African swine fever virus entry via caveola-mediated endocytic pathway.Journal of virology · 2026Article
- Efferocytosis of apoptotic bodies drives SARS-CoV-2 infection and macrophage inflammation.Nature communications · 2026Article
- Towards an Original Anti-ASFV Vaccine: Cellular Immunity Induced by Extracellular Vesicles Engineered with ASFV Proteins.Vaccines · 2026Article
- Mechanisms and functions of large extracellular vesicle biogenesis.Nature cell biology · 2026Review
- EV-D68 exploits clathrin-mediated endocytosis and compensatory macropinocytosis for cellular entry.Journal of virology · 2026Article
- The IFIT3 Protein of Porcine Induces Interferon Signaling and Inhibits the Early Gene Expression of African Swine Fever Virus.Viruses · 2026Article
- Mechanistic insights and therapeutic advances in antiviral strategies against African swine fever virus.Acta pharmaceutica Sinica. B · 2026Review
- Apoptotic extracellular vesicles act as master regulators of the bone healing niche.Journal of nanobiotechnology · 2026Review
- The ASFV CD2v protein inhibits apoptosis by inducing proteasomal degradation of BimJournal of virology · 2026Article
- Heparan sulfate as an attachment factor for ASFV is restricted by host HB-EGF.Cellular and molecular life sciences : CMLS · 2026Article
- Apoptotic extracellular vesicles: unveiling mechanisms, diverse functions, and biomedical implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Article
- African swine fever virus pEP364R acts as an important inflammatory-inducing factor to activate NLRP3 inflammasome-mediated pyroptosis by regulating DDX3X.PLoS pathogens · 2026Article
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
African swine fever virus (ASFV), a devastating pathogen to the worldwide swine industry, mainly targets macrophage/monocyte lineage, but how the virus enters host cells has remained unclear. Here, we report that ASFV utilizes apoptotic bodies (ApoBDs) for infection and cell-cell transmission. We show that ASFV induces cell apoptosis of primary porcine alveolar macrophages (PAMs) at the late stage of infection to productively shed ApoBDs that are subsequently swallowed by neighboring PAMs to initiate a secondary infection as evidenced by electron microscopy and live-cell imaging. Interestingly, the virions loaded within ApoBDs are exclusively single-enveloped particles that are devoid of the outer layer of membrane and represent a predominant form produced during late infection. The in vitro purified ApoBD vesicles are capable of mediating virus infection of naive PAMs, but the transmission can be significantly inhibited by blocking the "eat-me" signal phosphatidyserine on the surface of ApoBDs via Annexin V or the efferocytosis receptor TIM4 on the recipient PAMs via anti-TIM4 antibody, whereas overexpression of TIM4 enhances virus infection. The same treatment however did not affect the infection by intracellular viruses. Importantly, the swine sera to ASFV exert no effect on the ApoBD-mediated transmission but can partially act on the virions lacking the outer layer of membrane. Thus, ASFV has evolved to hijack a normal cellular pathway for cell-cell spread to evade host responses.
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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.