IFN-λ prevents influenza virus spread from the upper airways to the lungs and limits virus transmission.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 29651984.
- Also identified by DOI 10.7554/eLife.33354 and PMC identifier 5953542.
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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 (<i>Ifnlr1<sup>-/-</sup></i>) no longer restricted virus dissemination from the upper airways to the lungs. <i>Ifnlr1<sup>-/-</sup></i> 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.
Medical subject headings
- Antiviral Agents
- Interferon-gamma
- Lung
- Orthomyxoviridae
- Orthomyxoviridae Infections
- Receptors, Interferon
- Respiratory System