Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity

Tzu Han Hsieh, Tsung Ting Tsai, Chia Ling Chen, Ting Jing Shen, Ming Kai Jhan, Po Chun Tseng, Chiou Feng Lin

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

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.

Original languageEnglish
Article number375
JournalFrontiers in cellular and infection microbiology
Volume10
DOIs
Publication statusPublished - Jul 28 2020

Keywords

  • DC-SIGN
  • dengue virus
  • IL-10
  • monocytes
  • senescence

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

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