In order to better understand Influenza A virus and how it spreads, University of Minnesota Medical School researchers took a closer look at infected cells in the respiratory tract. What they discovered is not only is the immune system response tuned to the amount of virus replication, it's also tuned to the viral spread. They believe this deeper and more accurate understanding of the influenza virus and how it spreads could be the building blocks to better protective therapies for patients in the future.
In a paper published earlier this month in PNAS, the team described their process as well as their findings. They first had to create a virus that could not spread—it could replicate but it could never get into a new cell. Once they accomplished this, they could then artificially look at virus spread, with the goal of studying how new infections changed after immune responses have started. They found that during virus spread, the second round of replication does not seriously infect ciliated cells, which means the body does a really good job protecting those cells. However other cells weren't protected at all, like type-one alveolar cells, which are the cells responsible for gas exchange.
"It's really important to know how cells protect themselves from viruses and how this protection can be imparted on different cell types," said the study's senior author Ryan Langlois, Ph.D., assistant professor in the department of microbiology and immunology. "Clearly its not equal. Why it isn't equal, what are the mechanisms driving this, and what this means for disease we don't know yet."