tetano
Editor, Senior Moderator
Elife. 2018 Apr 13;7. pii: e33354. doi: 10.7554/eLife.33354. [Epub ahead of print]
[h=1]IFN-λ prevents influenza virus spread from the upper airways to the lungs and limits virus transmission.[/h] Klinkhammer J[SUP]1[/SUP], Schnepf D[SUP]1[/SUP], Ye L[SUP]1[/SUP], Schwaderlapp M[SUP]1[/SUP], Gad HH[SUP]2[/SUP], Hartmann R[SUP]2[/SUP], Garcin D[SUP]3[/SUP], Mahlak?iv T[SUP]1[/SUP], Staeheli P[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]-/-[/SUP]) no longer restricted virus dissemination from the upper airways to the lungs. Ifnlr1[SUP]-/-[/SUP] mice shed significantly more infectious virus particles via the nostrils and transmitted the virus much more efficiently to na?ve 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 na?ve contacts.
[h=4]KEYWORDS:[/h] immunology; infectious disease; inflammation; microbiology; mouse; viruses
PMID: 29651984 DOI: 10.7554/eLife.33354
Free full text
[h=1]IFN-λ prevents influenza virus spread from the upper airways to the lungs and limits virus transmission.[/h] Klinkhammer J[SUP]1[/SUP], Schnepf D[SUP]1[/SUP], Ye L[SUP]1[/SUP], Schwaderlapp M[SUP]1[/SUP], Gad HH[SUP]2[/SUP], Hartmann R[SUP]2[/SUP], Garcin D[SUP]3[/SUP], Mahlak?iv T[SUP]1[/SUP], Staeheli P[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]-/-[/SUP]) no longer restricted virus dissemination from the upper airways to the lungs. Ifnlr1[SUP]-/-[/SUP] mice shed significantly more infectious virus particles via the nostrils and transmitted the virus much more efficiently to na?ve 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 na?ve contacts.
[h=4]KEYWORDS:[/h] immunology; infectious disease; inflammation; microbiology; mouse; viruses
PMID: 29651984 DOI: 10.7554/eLife.33354
Free full text