Axis of Coinfection Evil

Influenza has given us 2 opportunities within 5 years to critically evaluate our understanding of how infections caused by a relatively simple virus produce patho-physiologic mayhem and death. Concern about the potential devastating consequences of a species jump of H5N1 influenza virus from birds to humans stimulated extensive research on that virus, resulting in much new knowledge provided by investigators globally. In 2009, the world recognized another threatening viral event: the emergence and rapid spread of a reassortant H1N1 virus that has some genetic features of a swine flu virus and is the same serotype responsible for the 1918 flu pandemic blamed for the death of tens of millions. Because many who died in the 1918 pandemic had secondary lung infections caused by bacteria, as recently reaffirmed by painstaking analysis of autopsy records [1], it seemed prudent to gain enhanced understanding of the molecular mechanisms underlying this potentially devastating “one-two” microbial punch. It is against this backdrop that Lee et al [2] have produced the important work found in this issue of the Journal.