A bout with flu virus can be hard, but when Streptococcus pneumonia enters the mix, it can turn deadly.
Now researchers have found a further reason for the severity of this dual infection by identifying a new virulence mechanism for a surface protein on the pneumonia-causing bacteria S. pneumoniae. This insight comes more than three decades after discovery of that surface protein, called pneumococcal surface protein A, or PspA.
This new mechanism had been missed in the past because it facilitates bacterial adherence only to dead or dying lung epithelial cells, not to living cells. Heretofore, researchers typically used healthy lung cell monolayers to search for bacterial adhesins that aid infection. Virus killing of lung cells during flu was found to set the stage for S. pneumonia attachment to the airway, thereby worsening disease and pneumonia.
The research, published in the journal Cell Reports, was led by Carlos Orihuela, Ph.D., and David Briles, Ph.D., professor and professor emeritus in the University of Alabama at Birmingham Department of Microbiology. Orihuela and Briles say their findings provide further explanation for how an infection by influenza A flu virus — followed by S. pneumoniae superinfection — causes severe pneumonia and a high death rate. The mechanism also points to possible improvements for disease treatment and vaccination.
uab.edu/news/research/item/...
Cell Reports. Research Paper:
