SAN FRANCISCO, June 9 (Xinhua) -- Researchers at the University of California, Berkeley, have found that viral infections turn down the intensity of a key cell-signaling pathway linked to healing and health of skeletal muscle and bone, mental well-being and prevention of obesity.
While the findings were recently published online in the journal Skeletal Muscle, the signaling pathway, called oxytocin receptor MAPK, or OXTR, has been well studied for its role in trust and bonding and more recently was found to be needed for muscle maintenance and regeneration, which declines with age.
"Our results suggest that viral infections in general may play a role in decreasing muscle health and regeneration, a decline in metabolic health and a lower sense of well-being, as these rely on effective OXTR signaling," said Irina Conboy, an associate professor in the Department of Bioengineering, whose lab performed the study.
The unexpected effects of viral infections, which may explain why viruses can make people feel lousy, were discovered by the research team with a standard method for inserting genes inside cells and organisms, one that deploys viruses as tools of molecular biology.
Viral vectors are tools regularly used to insert pieces of genetic material into cells or animals for further testing.
To ensure that any observed effects are caused by the genetic material of interest, and not by the viral vector, an experimental step is to test the effects of the viral vectors alone.
This is called an experimental control, and the vectors tested are called control viral vectors, as they are not supposed to change anything in a cell or organism.
Yet the study's results show that cells and animals exposed to control viral vectors differ from unexposed organisms in a number of ways.
The researchers found that control viral vectors actually changed the intensity of OXTR signaling, which diminished the regenerative ability of any direct descendants of these cells or tissues, thus aging them rapidly.
In one experiment, OXTR declined by 70 percent in mouse and human muscle cells that were given the control viral vectors.
The researchers then tested how a downregulated OXTR pathway affected muscle cells, and found that control viral vectors decreased mouse muscle cell proliferation from 85 to 20 percent; and cells also lose a key marker of muscle stem cell proliferation.
The researchers also examined a database of human studies and found that OXTR becomes severely diminished in humans after viral infections compared to healthy individuals.
"Our study further implies that viral infections may play a role in decreasing OXTR and thus broadly interfering with regeneration and maintenance of multiple tissues," Conboy was quoted as saying in a news release from UC Berkeley.
