病毒
病毒学
干扰素
生物
呼吸道
甲型流感病毒
病毒复制
呼吸系统
传输(电信)
受体
正粘病毒科
免疫学
微生物学
工程类
电气工程
解剖
生物化学
作者
Jonas Klinkhammer,Daniel Schnepf,Liang Ye,Marilena Schwaderlapp,Hans Henrik Gad,Rune Hartmann,Dominique Garcin,Tanel Mahlakõiv,Peter Staeheli
出处
期刊:eLife
[eLife Sciences Publications, Ltd.]
日期:2018-04-13
卷期号:7
被引量:195
摘要
Host factors restricting the transmission of respiratory viruses are poorly characterized. We analyzed the contribution of type I and type III interferon (IFN) using a mouse model in which the virus is selectively administered to the upper airways, mimicking a natural respiratory virus infection. Mice lacking functional IFN-λ receptors (Ifnlr1−/−) no longer restricted virus dissemination from the upper airways to the lungs. Ifnlr1−/− mice shed significantly more infectious virus particles via the nostrils and transmitted the virus much more efficiently to naïve contacts compared with wild-type mice or mice lacking functional type I IFN receptors. Prophylactic treatment with IFN-α or IFN-λ inhibited initial virus replication in all parts of the respiratory tract, but only IFN-λ conferred long-lasting antiviral protection in the upper airways and blocked virus transmission. Thus, IFN-λ has a decisive and non-redundant function in the upper airways that greatly limits transmission of respiratory viruses to naïve contacts.
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