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Dynamic, Helminth-Induced Immune Modulation Influences the Outcome of Acute and Chronic Hepatitis B Virus Infection.
The Journal of Infectious Diseases ( IF 6.4 ) Pub Date : 2019-12-25 , DOI: 10.1093/infdis/jiz594
Eva Loffredo-Verde 1, 2 , Sonakshi Bhattacharjee 1 , Antje Malo 2 , Julia Festag 2 , Anna D Kosinska 2, 3 , Marc Ringelhan 3, 4 , Sabrina Rim Sarkar 5 , Katja Steiger 5 , Mathias Heikenwaelder 2, 6 , Ulrike Protzer 2, 3 , Clarissa U Prazeres da Costa 1, 3
Affiliation  

BACKGROUND Chronic hepatitis B develops more frequently in countries with high prevalence of helminth infections. The crosstalk between these 2 major liver-residing pathogens, Schistosoma mansoni and hepatitis B virus (HBV), is barely understood. METHODS We used state-of-the-art models for both acute and chronic HBV infection to study the pathogen-crosstalk during the different immune phases of schistosome infection. RESULTS Although liver pathology caused by schistosome infection was not affected by either acute or chronic HBV infection, S mansoni infection influenced HBV infection outcomes in a phase-dependent manner. Interferon (IFN)-γ secreting, HBV- and schistosome-specific CD8 T cells acted in synergy to reduce HBV-induced pathology during the TH1 phase and chronic phase of schistosomiasis. Consequently, HBV was completely rescued in IFN-γ-deficient or in TH2 phase coinfected mice demonstrating the key role of this cytokine. It is interesting to note that secondary helminth infection on the basis of persistent (chronic) HBV infection increased HBV-specific T-cell frequency and resulted in suppression of virus replication but failed to fully restore T-cell function and eliminate HBV. CONCLUSIONS Thus, schistosome-induced IFN-γ had a prominent antiviral effect that outcompeted immunosuppressive effects of TH2 cytokines, whereas HBV coinfection did not alter schistosome pathogenicity.

中文翻译:

动态,蠕虫诱导的免疫调节影响急性和慢性乙型肝炎病毒感染的结果。

背景技术在蠕虫感染高发的国家中,慢性乙型肝炎的发病率更高。人们几乎不了解这两种主要的肝脏病原体,曼氏血吸虫和乙型肝炎病毒(HBV)之间的串扰。方法我们使用了针对急性和慢性HBV感染的最新模型来研究血吸虫感染不同免疫阶段的病原体串扰。结果尽管由血吸虫感染引起的肝病理学不受急性或慢性HBV感染的影响,但曼氏S感染以阶段性方式影响HBV感染的结果。在血吸虫病的TH1期和慢性期,分泌干扰素(IFN)-γ的HBV和血吸虫特异性CD8 T细胞协同作用,以减少HBV诱导的病理。所以,HBV在IFN-γ缺陷或TH2期合并感染的小鼠中被完全拯救,证明了这种细胞因子的关键作用。有趣的是,在持续性(慢性)HBV感染的基础上,继发性蠕虫感染增加了HBV特异性T细胞频率,并导致病毒复制受到抑制,但未能完全恢复T细胞功能并消除HBV。结论因此,血吸虫诱导的IFN-γ具有明显的抗病毒作用,胜过TH2细胞因子的免疫抑制作用,而HBV合并感染并未改变血吸虫的致病性。有趣的是,在持续性(慢性)HBV感染的基础上,继发性蠕虫感染增加了HBV特异性T细胞频率,并导致病毒复制受到抑制,但未能完全恢复T细胞功能并消除HBV。结论因此,血吸虫诱导的IFN-γ具有明显的抗病毒作用,胜过TH2细胞因子的免疫抑制作用,而HBV合并感染并未改变血吸虫的致病性。有趣的是,在持续(慢性)HBV感染的基础上,继发性蠕虫感染增加了HBV特异性T细胞频率,并导致病毒复制受到抑制,但未能完全恢复T细胞功能并消除HBV。结论因此,血吸虫诱导的IFN-γ具有明显的抗病毒作用,胜过TH2细胞因子的免疫抑制作用,而HBV合并感染并未改变血吸虫的致病性。
更新日期:2020-04-17
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