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.

衰老和慢性病通常通过涉及免疫衰老的机制增加登革热病毒（DENV）感染的发生率；然而，改变细胞对病毒感染的敏感性的细胞衰老的替代作用仍然未知。用D-半乳糖处理以诱导细胞衰老的人单核THP-1细胞（ATCC TIB-202）容易感染DENV。这些衰老细胞显示出增加的病毒进入/结合，基因/蛋白质表达和dsRNA复制。复制子系统的使用表明，药理诱导的衰老并没有增强对病毒蛋白翻译的影响。通过检查病毒受体的表达，我们发现衰老细胞中CD209（DC-SIGN）的表达增加。白细胞介素（IL）-10是由衰老细胞大量产生的，并且在这些衰老细胞中，DENV受体DC-SIGN的表达增加了，部分是通过IL-10介导的JAK2-STAT3信号通路的调节。结果表明，衰老表型可能通过增加DC-SIGN表达来促进DENV感染。