The H1N1 flu has now been circulating for over 3 months and has landed on every continent (Antarctica doesn’t count as a continent in the medical world), infecting thousands of people. People continue to die at a steady pace and yesterday a girl in Brazil died with atypical symptoms (yes it is in Portuguese, but I’ll summarize what it says here).
This girl had contracted a pneumococcus infection and ended up dying from septicemia. The physicians speculate that her contraction of H1N1 may have lowered her immunity to a pneumonia infection, leaving her vulnerable to the bacteria.
Although the science is still out on this issue there is a model that has been presented about why those infected with influenza are at an increased risk for secondary pneumococcus infections. An article in the Journal of Clinical Investigation seems to pinpoint the reason for the increased risk of secondary infection.
The scientists proposed that when the body responds to a viral infection there is a concurrent loss in the ability to respond to bacterial infections. Type I IFN receptors were targeted because they are a large part of the innate response to viral infections. When activated they produce a cascade of cytokines that act to inhibit viral replication. This is the early response the body takes as it goes through the process of antibody production and maturation (maybe one of the most fascinating subjects in immunology). The researchers found that when mice had their Type I IFN receptors knocked out there was a much higher level of KC and Mip2, two chemoattractants used to recruit neutrophils to the site of bacterial infection.
So it looks as though the Type I IFN receptors inhibit the production of KC and Mip2. This would cause far less neutrophils to be found at infection sites in mice responding to an influenza challenge, which is what the researchers saw.
This is another key in developing a model of how one branch of the immune response can mediate activity of another branch of the system. It is complicated though as it has been shown that influenza proteins can inhibit the production of IFN, which would also inhibit the activation of the IFN receptors and subsequent products.
Secondary pneumococcal infection also only occurs in a subset of individuals so there are still parts of this story that need to be elucidated. But this does give immunologists a working model for this system of infections and as can be seen from the case in Brazil maybe help to stop further infections in the future.
Shahangian, A., Chow, E., Tian, X., Kang, J., Ghaffari, A., Liu, S., Belperio, J., Cheng, G., & Deng, J. (2009). Type I IFNs mediate development of postinfluenza bacterial pneumonia in mice Journal of Clinical Investigation, 119 (7), 1910-1920 DOI: 10.1172/JCI35412