Researchers are reporting new evidence that a certain type of lung cell develops an enhanced ability to repair damaged DNA and survive an influenza attack while other cells around it die. A better understanding of this self-repair mechanism provides new insights into the viral infection process and may represent a promising antimicrobial strategy for the future, they say. It may also provide new clues for fighting a variety of respiratory disease including COPD and asthma.
The resistant cell is called a club cell, which is found in narrow airways just above the alveoli of the lungs where gases are exchanged. The cell normally produces surfactants and secretes various proteins that coat the lining of the lungs. The function of these cells during infection is poorly understood.
In recent studies, the research team showed that club cells could survive a flu infection that would kill most cells. In the new study, the researchers reveal a mechanism that may help explain why. While sorting through all of the club cell’s viral response pathways during infection, they demonstrated in lab studies that the club cells increase their efforts to repair DNA damage in response to infection. The net result is that the lungs will remain resistant to new viruses even after an infection has cleared, the researchers say.
The study, which was partially funded by NHLBI, appeared in Nature Microbiology.