Influenza A viruses (IAVs) are zoonotic pathogens that sometimes establish long-term lineages in humans and other mammalian hosts. New introductions of influenza genes or whole viruses from animal reservoirs can result in viruses with an exceptionally virulent phenotype. After a period of adaptation and development of population immunity, however, the descendents of pandemic viruses rarely cause severe illness and mortality through direct viral damage in immunocompetent hosts [1, 2]. Instead, exacerbation of a preexisting, chronic illness or virus-mediated impairment of host defenses facilitating bacterial superinfection account for most fatalities. Selwyn Collins of the US Public Health Service, who refined the terms by which we classify outcomes after influenza, expressed this view as, “In fact, influenza may well be thought of as not a killing disease except by the intervention of pneumonia or the presence of chronic disease in a patient” [3].

Influenza B viruses (IBVs) are stably adapted to humans, having diverged from IAVs at some point in the distant past. IBVs were first isolated from humans in 1940 and have caused seasonal epidemics since at least 1935 but likely have been endemic in humans for centuries. Although IBVs can establish lineages in seals, they are not known to have a stable animal reservoir from which new variants could emerge [4]. Over the last several decades, rates of hospitalization and mortality attributed to IBVs have been lower than those associated with H3N2 subtype IAVs but higher than those linked to the less virulent seasonal H1N1 strains. During the 2010–2011 season, 38% of all influenza-associated pediatric deaths were attributed to IBVs, despite only 26% of all circulating viruses being of this type [5]. Half (49%) of these children who died had no known high-risk medical condition, and only 50% received any …