The W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Virology. 2010 Apr 25;400(1):115-27. doi: 10.1016/j.virol.2010.01.027. Epub 2010 Feb 18.
Hantavirus infection reduces antiviral defenses, increases regulatory responses, and causes persistent infection in rodent hosts. To address whether hantaviruses alter the maturation and functional activity of antigen presenting cells (APCs), rat bone marrow-derived dendritic cells (BMDCs) and macrophages (BMDMs) were generated and infected with Seoul virus (SEOV) or stimulated with TLR ligands. SEOV infected both DCs and macrophages, but copies of viral RNA, viral antigen, and infectious virus titers were higher in macrophages. The expression of MHCII and CD80, production of IL-6, IL-10, and TNF-alpha, and expression of Ifnbeta were attenuated in SEOV-infected APCs. Stimulation of APCs with poly I:C prior to SEOV infection increased the expression of activation markers and production of inflammatory cytokines and suppressed SEOV replication. Infection of APCs with SEOV suppressed LPS-induced activation and innate immune responses. Hantaviruses reduce the innate immune response potential of APCs derived from a natural host, which may influence persistence of these zoonotic viruses in the environment.
汉坦病毒感染会降低抗病毒防御能力，增加调节反应，并导致啮齿动物宿主持续感染。为了研究汉坦病毒是否会改变抗原呈递细胞（APCs）的成熟和功能活性，我们生成了大鼠骨髓来源的树突状细胞（BMDCs）和巨噬细胞（BMDMs），并用首尔病毒（SEOV）感染或用 TLR 配体刺激。SEOV 可感染 DC 和巨噬细胞，但病毒 RNA、病毒抗原和感染性病毒滴度在巨噬细胞中更高。SEOV 感染的 APCs 中 MHCII 和 CD80 的表达、IL-6、IL-10 和 TNF-α的产生以及 Ifnbeta 的表达均减弱。在 SEVO 感染前用 poly I:C 刺激 APCs 会增加激活标志物的表达和炎症细胞因子的产生，并抑制 SEVO 的复制。SEOV 感染会抑制 LPS 诱导的 APC 激活和先天免疫反应。汉坦病毒降低了源自天然宿主的 APC 的固有免疫反应潜力，这可能会影响这些人畜共患病病毒在环境中的持续存在。
