| First Author | Klinkhammer J | Year | 2018 |
| Journal | Elife | Volume | 7 |
| PubMed ID | 29651984 | Mgi Jnum | J:264163 |
| Mgi Id | MGI:6191815 | Doi | 10.7554/eLife.33354 |
| Citation | Klinkhammer J, et al. (2018) IFN-lambda prevents influenza virus spread from the upper airways to the lungs and limits virus transmission. Elife 7:e33354 |
| abstractText | 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 IFN-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. |
