IFN-λ prevents influenza virus spread from the upper airways to the lungs and limits virus transmission.

ABSTRACT: 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 respirator

SUBMITTER: Klinkhammer J 

PROVIDER: S-EPMC5953542 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature