Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity
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 (AT...
Main Authors: | , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Frontiers Media S.A.
2020-07-01
|
Series: | Frontiers in Cellular and Infection Microbiology |
Subjects: | |
Online Access: | https://www.frontiersin.org/article/10.3389/fcimb.2020.00375/full |
_version_ | 1811333431580164096 |
---|---|
author | Tzu-Han Hsieh Tsung-Ting Tsai Chia-Ling Chen Ting-Jing Shen Ting-Jing Shen Ming-Kai Jhan Ming-Kai Jhan Po-Chun Tseng Po-Chun Tseng Chiou-Feng Lin Chiou-Feng Lin Chiou-Feng Lin Chiou-Feng Lin |
author_facet | Tzu-Han Hsieh Tsung-Ting Tsai Chia-Ling Chen Ting-Jing Shen Ting-Jing Shen Ming-Kai Jhan Ming-Kai Jhan Po-Chun Tseng Po-Chun Tseng Chiou-Feng Lin Chiou-Feng Lin Chiou-Feng Lin Chiou-Feng Lin |
author_sort | Tzu-Han Hsieh |
collection | DOAJ |
description | 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. |
first_indexed | 2024-04-13T16:51:41Z |
format | Article |
id | doaj.art-031c8e2a043f4edea7cd06d03a087043 |
institution | Directory Open Access Journal |
issn | 2235-2988 |
language | English |
last_indexed | 2024-04-13T16:51:41Z |
publishDate | 2020-07-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Cellular and Infection Microbiology |
spelling | doaj.art-031c8e2a043f4edea7cd06d03a0870432022-12-22T02:38:55ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882020-07-011010.3389/fcimb.2020.00375557664Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing InfectivityTzu-Han Hsieh0Tsung-Ting Tsai1Chia-Ling Chen2Ting-Jing Shen3Ting-Jing Shen4Ming-Kai Jhan5Ming-Kai Jhan6Po-Chun Tseng7Po-Chun Tseng8Chiou-Feng Lin9Chiou-Feng Lin10Chiou-Feng Lin11Chiou-Feng Lin12Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanDepartment of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, TaiwanDepartment of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, TaiwanDepartment of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, TaiwanDepartment of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanCore Laboratory of Immune Monitoring, Office of Research and Development, Taipei Medical University, Taipei, TaiwanDepartment of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, TaiwanCore Laboratory of Immune Monitoring, Office of Research and Development, Taipei Medical University, Taipei, TaiwanCenter of Infectious Diseases and Signaling Research, National Cheng Kung University, Tainan, TaiwanAging 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.https://www.frontiersin.org/article/10.3389/fcimb.2020.00375/fulldengue virussenescenceIL-10DC-SIGNmonocytes |
spellingShingle | Tzu-Han Hsieh Tsung-Ting Tsai Chia-Ling Chen Ting-Jing Shen Ting-Jing Shen Ming-Kai Jhan Ming-Kai Jhan Po-Chun Tseng Po-Chun Tseng Chiou-Feng Lin Chiou-Feng Lin Chiou-Feng Lin Chiou-Feng Lin Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity Frontiers in Cellular and Infection Microbiology dengue virus senescence IL-10 DC-SIGN monocytes |
title | Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity |
title_full | Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity |
title_fullStr | Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity |
title_full_unstemmed | Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity |
title_short | Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity |
title_sort | senescence in monocytes facilitates dengue virus infection by increasing infectivity |
topic | dengue virus senescence IL-10 DC-SIGN monocytes |
url | https://www.frontiersin.org/article/10.3389/fcimb.2020.00375/full |
work_keys_str_mv | AT tzuhanhsieh senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT tsungtingtsai senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT chialingchen senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT tingjingshen senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT tingjingshen senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT mingkaijhan senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT mingkaijhan senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT pochuntseng senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT pochuntseng senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT chioufenglin senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT chioufenglin senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT chioufenglin senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity AT chioufenglin senescenceinmonocytesfacilitatesdenguevirusinfectionbyincreasinginfectivity |