ArticleFrontiers in cellular and infection microbiology2020
Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity.
Article in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Decoding antidengue serotype-3 (DENV-3) mechanism of natural glycosides fromOpen veterinary journal · 2026Article
- Senolytic Treatment Reduces Acute and Chronic Lung Inflammation in an Aged Mouse Model of Influenza.Aging cell · 2026Article
- Dengue and severe dengue.Clinical microbiology reviews · 2025Review
- Clinical application of mesenchymal stem cells in immunosenescence: a qualitative review of their potential and challenges.Stem cell research & therapy · 2025Review
- [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- Reconciling heterogeneous dengue virus infection risk estimates from different study designs.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Reconciling heterogeneous dengue virus infection risk estimates from different study designs.medRxiv : the preprint server for health sciences · 2024Article
- DNA damage response(DDR): a link between cellular senescence and human cytomegalovirus.Virology journal · 2023Review
- Removal of senescent cells reduces the viral load and attenuates pulmonary and systemic inflammation in SARS-CoV-2-infected, aged hamsters.Nature aging · 2023Article
- Radiation-Induced Cellular Senescence Reduces Susceptibility of Glioblastoma Cells to Oncolytic Vaccinia Virus.Cancers · 2023Article
- COVID-19 and cellular senescence.Nature reviews. Immunology · 2023Review
- Interactomics: Dozens of Viruses, Co-evolving With Humans, Including the Influenza A Virus, may Actively Distort Human Aging.Molecular biology and evolution · 2023Article
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- Review
- Assessing the role of multiple mechanisms increasing the age of dengue cases in Thailand.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Cell Strain-Derived Induced Pluripotent Stem Cells as an Isogenic Approach To Investigate Age-Related Host Response to Flaviviral Infection.Journal of virology · 2022Article
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- Potential of Mesenchymal Stem Cells in the Rejuvenation of the Aging Immune System.International journal of molecular sciences · 2021Review
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging and chronic condition increase the incidence of dengue virus (DENV) infection, generally through a mechanism involving immunosenescence; however, the alternative effects of cellular senescence, which alters cell susceptibility to viral infection, remain unknown. Human monocytic THP-1 cells (ATCC TIB-202) treated with D-galactose to induce cellular senescence were susceptible to DENV infection. These senescent cells showed increased viral entry/binding, gene/protein expression, and dsRNA replication. The use of a replicon system showed that pharmacologically induced senescence did not enhance the effects on viral protein translation. By examining viral receptor expression, we found increased expression of CD209 (DC-SIGN) in the senescent cells. Interleukin (IL)-10 was aberrantly produced at high levels by the senescent cells, and the expression of the DENV receptor DC-SIGN was increased in these senescent cells, partially via IL-10-mediated regulation of the JAK2-STAT3 signaling pathway. The results demonstrate that a senescent phenotype facilitates DENV infection, probably by increasing DC-SIGN expression.
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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.