Close Encounters of the Viral Kind: Cross‐Kingdom Synergies at the Host–Pathogen Interface

Abstract

The synergies between viral and bacterial infections are well established. Most studies have been focused on the indirect mechanisms underlying this phenomenon, including immune modulation and alterations to the mucosal structures that promote pathogen outgrowth. A growing body of evidence implicates direct binding of virus to bacterial surfaces being an additional mechanism of synergy at the host-pathogen interface. These cross-kingdom interactions enhance bacterial and viral adhesion and can alter tissue tropism. These bacterial-viral complexes play unique roles in pathogenesis and can alter virulence potential. The bacterial-viral complexes may also play important roles in pathogen transmission. Additionally, the complexes are recognized by the host immune system in a distinct manner, thus presenting novel routes for vaccine development. These synergies are active for multiple species in both the respiratory and gastrointestinal tract, indicating that direct interactions between bacteria and virus to modulate host interactions are used by a diverse array of species.

Secondary streptococcal infection following influenza

“…Recent studies have revealed that the high mortality caused by the Spanish influenza was due to bacterial pneumonia combined with influenza or bacterial pneumonia following influenza 2–5 . The viral–bacterial complexes play unique roles in pathogenesis and can alter virulence potential 6 . IAV infection has been shown to enhance susceptibility to a secondary bacterial infection 2,4,5,7–10 .…”

“…A number of excellent reviews regarding S. pneumoniae secondary infection following influenza have been presented 4–6,9,13–15 . However, other streptococci including pathogenic Streptococcus pyogenes (group A streptococcus ) and commensal streptococci (oral mitis group streptococci) also colonize in the upper respiratory tract in various ways (Figure 1).…”

“…[2][3][4][5] The viral-bacterial complexes play unique roles in pathogenesis and can alter virulence potential. 6 IAV infection has been shown to enhance susceptibility to a secondary bacterial infection. 2,4,5,[7][8][9][10] Because IAV infects the upper respiratory tract (nasal cavity, oral cavity, pharynx), bacteria that colonize in or infect the upper respiratory tract must be major contributors to co-and/or secondary infection.…”

“…7,8,11,12 A number of excellent reviews regarding S. pneumoniae secondary infection following influenza have been presented. [4][5][6]9,[13][14][15] However, other streptococci including pathogenic Streptococcus pyogenes (group A streptococcus) and commensal streptococci (oral mitis group streptococci) also colonize in the upper respiratory tract in various ways (Figure 1). Although many studies have investigated the mechanism of representative secondary pneumonia by S. pneumoniae, additional findings regarding co-and/or secondary infection by S. pyogenes and oral mitis group streptococci will confer new insight into IAV-streptococcal synergic infection.…”