New research from Rockefeller University and collaborators have found interesting insight into the way our body turns the tables on viruses like the Flu, or Influenza A.
A study led by researcher Charles Rice, head of the Laboratory of Virology and Infectious Disease, shows how viruses like Influenza A is combated by the immune system response of shutting down its own protein- splicing mechanisms to inhibit any further growth and spreading of the infection throughout the cells.
A virus must have a host to thrive and often times a virus puts the majority of its “trust” into our body’s fundamental functions of reproducing new cells. Without this reproduction of new cells, the virus cannot reproduce. This is why viruses attack and thrive in living organisms who fit the criteria of either rapid-cell producing organisms, the young, or hosts who have weak immune defenses; the old.
The research shows however, that this tactical approach by the infecting viruses also makes the virus very vulnerable to failure if the host it’s attacking shuts down the cells ability to reproduce. The study shows how this vulnerability has can be exploited by a specific protein shutting down its routine functions. This protein is called PAI-1 or Plasminogen Activator Inhibitor 1. This protein is best known for its function in breaking down proteases. Proteases are enzymes that break the chemical bonds inside protein molecules. What happens is PAI-1 steps in and stops proteases from performing this task, inhibiting the further breakdown of chemical bonds.
This defensive mechanism seen in PAI-1 led the scientist’s curiosity to see if the protein would do the same when a cell became infected with a virus. Researchers started taking a closer look at PAI-1 in conjunction with a virus infection in human cells and mice cells and they noted that subjects whom had less ability to produce PAI-1, were far more vulnerable to Influenza-A infections.
After this realization, the Scientists performed their experiment using samples of both human and mice cells and infected them with the subtype H1N1, a popular member of a large family of flu viruses. H1N1 also being a derivative of the pandemic flu of 1918 and the often deadly flu today, Influenza-A.
Because it takes 8 hours for Influenza A’s to complete its replication cycle and exit the cell, the researchers watched during this time for which specific genes would inhibit further spread. Many genes go to battle when they sense an infection that is trying to replicate, but the one that stood out above all the rest was SERPINE1, the gene that codes for PAI-1.
Following this finding, researchers went through existing databases of patients whom had succumbed to a virus infection like Influenza A or other viruses similar in that the virus depended on its host for proteases to complete replication. Not surprisingly, they discovered that the patients with mutated SERPINE1 genes (which don’t produce high levels of PAI-1), were heavily impacted by viral infections.
This study opens up the possibility that similar strategies like seen with PAI-1 could yield a new treatment for the flu as well as other viral infections.
Read more about this new discovery by Rockefeller University by following the link.
Image Courtesy of: Boston Magazine