Secondary streptococcal infection following influenza

Abstract Secondary bacterial infection following influenza type A virus (IAV) infection is a major cause of morbidity and mortality during influenza epidemics. Streptococcus pneumoniae has been identified as a predominant pathogen in secondary pneumonia cases that develop following influenza. Although IAV has been shown to enhance susceptibility to the secondary bacterial infection, the underlying mechanism of the viral–bacterial synergy leading to disease progression is complex and remains elusive. In this review, cooperative interactions of viruses and streptococci during co‐ or secondary infection with IAV are described. IAV infects the upper respiratory tract, therefore, streptococci that inhabit or infect the respiratory tract are of special interest. As many excellent reviews on the co‐infection of IAV and S. pneumoniae have already been published, this review is intended to describe the unique interactions between other streptococci and IAV. Both streptococcal and IAV infections modulate the host epithelial barrier of the respiratory tract in various ways. IAV infection directly disrupts epithelial barriers, though at the same time the virus modifies the properties of infected cells to enhance streptococcal adherence and invasion. Mitis group streptococci produce neuraminidases, which promote IAV infection in a unique manner. The studies reviewed here have revealed intriguing mechanisms underlying secondary streptococcal infection following influenza.