The scientific journal, “Kinetics of coinfection with Influenza A Virus and Streptococcus pneumoniae,” discusses the influences of combining the influenza virus with another bacteria, S. pneumonia. According to the journal, influenza can be transformed from a slight infection into a fierce or fatal virus when S. pneumoniae is incorporated into the environment near the virus. Some aspects of both influenza and S. pneumoniae infecting an organism consist of inflammation and airway impairment. The similarities between the two viruses could be because both influenza and pneumococcus make use of identical pathways, cofactors and intermediates. The influenza virus works by diminishing the immune systems responses to a virus, and pneumococcus bacteria is better able to enter a cell when the immune system is not functioning properly. Exactly how this takes place is currently unknown, but the study conducted aids in further ...view middle of the document...
The mathematical model used to measure the cell activity was a target cell limited model with an eclipse phase for the influenza virus, and the S. pneumoniae infection was studied using a model of the first connection with the bacteria and the alveolar macrophages. The final model was derived from mechanisms of interaction between the two infections.
Previous research showed viral titers strengthened after addition of the bacteria and then gradually declined, but the bacterial titers were recorded to quickly rise and stay at high levels. The PR8 and PR8-PBI-F2(1918) strains of the influenza virus showed a viral titer increase of 3 with the PR8 virus and a 2.5 increase for PR8-PB1-F2(1918) when bacteria was added. The kinetic study showed an increase in adherence to cell tissue, virus production, and bacterial carrying capacity. They also showed a decrease in phagocytosis and immune responses.
The hypothesis stated that with the addition of bacteria, viral titers would rebound because infected cells were more likely to activate viral release. The cause of bacterial titers was suspected to be due to alveolar macrophage impairment. Alveolar macrophages keep the lungs clean by transporting both feasible and nonviable particles out of the cells located in the lungs, and these particles enter through the air that you breathe.
The results showed that the bacterial titers did seem to be involved with alveolar macrophage impairment, but viral titers did not significantly seem to prompt more viral release from infected cells. The increase of viral titers in both viral infections could be evidence of an intense viral inflation, but it was concluded that further research using the journal results would need to be done. The increase could just be initial interaction the bacteria have with the virus. Phagocytosis levels may be irrelevant to the study because when a large amount of S. pneumoniae was added, no matter how many bacteria were removed, there was still a large amount of bacteria growing in the cell. The change in the amount of pneumonococcus added and strain of the bacteria and virus seemed to influence how mild or fatal the coinfection became.