Fig. 1: Type I interferons are deleterious during neonatal influenza virus infection, while type III interferons are essential to protection.

Three-day old neonatal and 8-week-old adult mice were intranasally infected with PR8 influenza A virus. a Wild-type (dashed line) (n = 31) and IFNαβR^−/− (solid line) (n = 46) neonates were infected and tracked for survival (5 total independent experiments at 2 separate vivarium, 3 experiments performed at Drexel University (DU) and 2 experiments performed at Biomedical Research Foundation Academy of Athens(BRFAA) b At DU, 8-week-old wild-type (open circle) (n = 12, 3 independent experiments) and IFNαβR^−/− (closed circle) (n = 15, 4 independent experiments) mice were intranasally infected with PR8 influenza A virus and weights were tracked. Viral burden was determined at 1-, 3-, and 6- days post-infection by real-time PCR and is reported as the fold change relative to a 1-day post-infection wild-type neonatal mouse for c IFNαβR^−/− and e Ifnlr1^−/− neonatal mice. d At BRFAA, wild-type (dashed line) (n = 9, 2 separate experiments) and Ifnlr1^−/− (black line) (n = 12, 2 independent experiments) and IFNαβR^−/− Ifnlr1^−/− (blue line) (n = 14, 2 independent experiments) neonates were infected and tracked for survival. For viral load analysis, protocol 1 was used for IFNαβR^−/− at DU and protocol 2 was used for Ifnlr1^−/− at BRFAA. Statistical differences between wild type and transgenic animal survival were assessed by using log-rank (Mantel–Cox) test and Mann-Whitney test when comparing nonparametric values for viral loads and weight loss, where denoted *p < 0.05, ****p < 0.0001.