This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Researchers have figured out a missing piece of the puzzle of how human cells detect invading viruses and mount an immune response within an hour. This new insight into the battle between viruses and hosts could provide clues for improving vaccines, gene therapies and other treatments that use viruses to deliver medicines or fight disease themselves, the researchers said.
The findings were published Aug. 18 in Proceedings of the National Academy of Sciences. "It's important to understand the details of how viruses and the body's immune system interact, because those details give us a better idea of how we can use the same techniques to build better medicines," said senior author David Knipe, the Higgins Professor of Microbiology and Molecular Genetics in the Blavatnik Institute at Harvard Medical School. "Answering chains of puzzling questions without obvious, immediate utility enables us to engineer unexpected mechanisms we wouldn't have been able to conceive of otherwise," added Knipe, who has been studying the contest between herpesvirus and the immune system at the cellular and molecular level for decades.
Knipe and colleagues found that when a class of viruses known as enveloped viruses enter a cell by fusing with its outer membrane, tremors in the cell's scaffolding cause ruptures in the membrane of the cell nucleus, allowing DNA to leak into the cell body. DNA-detecting proteins known as cGAS then initiate an immune response to fight the virus. Researchers who study viruses coated in a fatty envelope, like herpes simplex virus, have long known that the body sends interferon to fight off infection within an hour of a virus entering a cell.
They have also known that a protein called cGAS, which detects loose segments of DNA in the cell body, activates the response. But many details of the process have remained mysterious. First, where does the DNA that triggers the response come from?
There were many hypotheses. One held that some virus particles burst after entering the cell but before reaching the cell nucleus, where they can hijack the cell's genetic machinery to replicate. Second, if viral DNA is the trigger, how can cGAS's response to infection by RNA viruses, which don't even have DNA, be explained?
Could it be host-cell DNA? If so, what causes DNA to spill out of the nucleus during viral entry? The researchers—led by first author Nicolás Romero, then a postdoctoral fellow in the Knipe Lab and now at Tufts University—conducted a series of experiments using human cell cultures and a herpesvirus modified so it could not replicate independently.
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