ArticleViruses2015
Coxsackievirus B4 Can Infect Human Peripheral Blood-Derived Macrophages.
Article in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Ajwa date extract (Saudi medical journal · 2025Article
- Macrophage-Specific Coxsackievirus and Adenovirus Receptor Deletion Enhances Macrophage M1 Polarity in CVB3-Induced Myocarditis.International journal of molecular sciences · 2023Article
- Viral infection-related gene upregulation in monocytes in children with signs of β-cell autoimmunity.Pediatric diabetes · 2022Article
- Persistent coxsackievirus B infection and pathogenesis of type 1 diabetes mellitus.Nature reviews. Endocrinology · 2022Review
- Enteroviruses and Type 1 Diabetes: Multiple Mechanisms and Factors?Annual review of medicine · 2022Review
- Concomitant pyroptotic and apoptotic cell death triggered in macrophages infected by Zika virus.PloS one · 2022Article
- Effect of Coxsackievirus B4 Infection on the Thymus: Elucidating Its Role in the Pathogenesis of Type 1 Diabetes.Microorganisms · 2021Review
- Coxsackievirus-B4 Infection Can Induce the Expression of Human Endogenous Retrovirus W in Primary Cells.Microorganisms · 2020Article
- Enteroviral Pathogenesis of Type 1 Diabetes: The Role of Natural Killer Cells.Microorganisms · 2020Review
- Pancreatic beta cells persistently infected with coxsackievirus B4 are targets of NK cell-mediated cytolytic activity.Cellular and molecular life sciences : CMLS · 2020Article
- Human Endogenous Retroviruses and Type 1 Diabetes.Current diabetes reports · 2019Review
- The heterogeneous pathogenesis of type 1 diabetes mellitus.Nature reviews. Endocrinology · 2019Review
- Monocytes and Macrophages as Viral Targets and Reservoirs.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beyond acute infections, group B coxsackieviruses (CVB) are also reported to play a role in the development of chronic diseases, like type 1 diabetes. The viral pathogenesis mainly relies on the interplay between the viruses and innate immune response in genetically-susceptible individuals. We investigated the interaction between CVB4 and macrophages considered as major players in immune response. Monocyte-derived macrophages (MDM) generated with either M-CSF or GM-CSF were inoculated with CVB4, and infection, inflammation, viral replication and persistence were assessed. M-CSF-induced MDM, but not GM-CSF-induced MDM, can be infected by CVB4. In addition, enhancing serum was not needed to infect MDM in contrast with parental monocytes. The expression of viral receptor (CAR) mRNA was similar in both M-CSF and GM-CSF MDM. CVB4 induced high levels of pro-inflammatory cytokines (IL-6 and TNFα) in both MDM populations. CVB4 effectively replicated and persisted in M-CSF MDM, but IFNα was produced in the early phase of infection only. Our results demonstrate that CVB4 can replicate and persist in MDM. Further investigations are required to determine whether the interaction between the virus and MDM plays a role in the pathogenesis of CVB-induced chronic diseases.
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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.