Most of our understanding of influenza A virus and its interaction with the adaptive immune response has been generated in the context of infection with a single pathogen. It is clear however that infection with influenza virus can lead to increased susceptibility to subsequent infection, often Streptococcus pneumoniae. The potential for a second infection to regulate the ongoing anti-influenza response is not clear. To address this important question we have developed an in vivo co-infection model to test the effects of pneumococcus on the ongoing CD8+ influenza specific T cell response. We show that co-infection with A/PR 8/34 (H1N1) and the non-invasive EF3030 strain of S. pneumoniae leads to increased disease. Within the lungs of the co-infected animals we observe a significant decrease in the size of the flu specific CD8+ T cell response. This decrease is not present in the lung draining lymph nodes, indicating selective regulation at the site of bacterial/viral co-infection. In addition to the decrease in size, the effector function of these CD8+ T cells is qualitatively diminished as measured by their ability to co-produce interferon γ and tissue necrosis factor α. These results demonstrate a dynamic interplay between the two concurrent pathogens and the immune system and emphasize the importance of increasing our understanding of how polymicrobial infections modulate the immune response to individual pathogens.
- Copyright © 2013 by The American Association of Immunologists, Inc.