Viruses are intracellular parasites that cause disease by infecting the cells in the body and, in a study published today in Nature Microbiology, researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine showed how a common virus hijacks a host cell's protein to help assemble new viruses before they are released. The findings increase our understanding of how viruses reproduce in the body and could lead to new therapeutics.
While most research into viral infections has focused on mechanisms viruses use to enter cells, less is known about the late steps in infection. The new findings were identified in reovirus, a common virus that is normally harmless but has recently been implicated as a potential cause of celiac disease.
"Our work provides compelling evidence that reoviruses, and perhaps additional distantly related viruses, require a specialized protein-folding machine expressed in cells to replicate," said Terence Dermody, M.D., chair of the Department of Pediatrics at Pitt's School of Medicine, physician-in-chief and scientific director at Children's Hospital, and the senior author on the study. "This is a pretty remarkable finding because viruses are in large part made of complex protein building blocks and we know little about how these blocks are assembled."
More information: Jonathan J. Knowlton et al, The TRiC chaperonin controls reovirus replication through outer-capsid folding, Nature Microbiology (2018). DOI: 10.1038/s41564-018-0122-x
Cells infected with reovirus (pink globules). Credit: Nature Microbiology/Dermody Lab
