期刊
ELIFE
卷 7, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.33354
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资金
- Novo Nordisk [NNF150C0017902]
- Danish Council for Independent Research-Medical Research [11-107588]
- Schweizerischer Nationalfonds zur Forderung der Wissenschaftlichen Forschung [31003A_163129]
- Deutsche Forschungsgemeinschaft [STA 338/15-1]
- European Commission UniVacFlu
- Swiss National Science Foundation (SNF) [31003A_163129] Funding Source: Swiss National Science Foundation (SNF)
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-lambda, 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 naive contacts compared with wild-type mice or mice lacking functional type I IFN receptors. Prophylactic treatment with IFN-alpha or IEN-lambda inhibited initial virus replication in all parts of the respiratory tract, but only IFN-lambda conferred long-lasting antiviral protection in the upper airways and blocked virus transmission. Thus, IFN-lambda has a decisive and non-redundant function in the upper airways that greatly limits transmission of respiratory viruses to naive contacts.
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