Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses.

Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wild-type SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are scarce. Here we demonstrate that SARS-CoV-2 infection induces a type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Furthermore, we show that physiological levels of IFNα detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells.

Comparative Immunogenicity of the 2014-2015 Northern Hemisphere Trivalent IIV and LAIV against Influenza A Viruses in Children.

Both inactivated influenza vaccines (IIV) and live-attenuated influenza vaccines (LAIV) have been recommended for administration to children. Children are a high-risk group for severe influenza, and a major source of transmission. Therefore, prevention of infection by vaccination is particularly important. However, efficacy and immunogenicity of these vaccines are known to vary by season and geographic location. We compared the immunogenicity of the 2014-2015 Northern Hemisphere trivalent IIV and LAIV against influenza A virus in Canadian Hutterite children aged 2 to 17 using hemagglutination inhibition (HAI) assays, and enzyme-linked immunosorbent assays to measure hemagglutinin-specific serum IgA and mucosal IgA. Both vaccine formulations induced significant increases in HAI titers against H1N1 and H3N2 vaccine strains. Serum IgA titers against H3N2 were significantly boosted by both IIV and LAIV, while only IIV induced a significant increase in serum IgA specific to the H1N1 vaccine strain. While HAI titers correlated with protection conferred by IIV, mucosal IgA titers correlated with protection conferred by LAIV (mucosal IgA titers could not be established as a correlate for IIV due to sample size limitations). IIV and LAIV were previously reported to be equally efficacious in this cohort, although the immunogenicity of IIV was generally superior.