New finding could pave the way towards better understanding of the body’s response to norovirus infection
Researchers led by the University of Surrey have found the first evidence of host protein synthesis regulation in norovirus infection – a significant cause of gastroenteritis outbreaks worldwide.
Scientists have previously shown that viruses can alter the activity of the cellular protein synthesis factory to favour virus propagation. In this new study, published in the Journal of Biological Chemistry, scientists from the University of Surrey, University of Cambridge and University of Sussex have discovered how it works by identifying the mechanism by which norovirus regulates the activity of a key component of the protein synthesis machinery, eIF4E. Researchers believe this finding could pave the way towards better understanding of the body’s response to norovirus infection and lead to new treatments against viruses.
The BBSRC-sponsored research revealed that a specific cascade of cellular signalling events, similar to traffic lights regulating the cell life, is activated during norovirus infection to modulate the activity of eIF4E and protein synthesis in the infected cell. This then leads to an increase in viral replication.
The scientists concluded that norovirus replication is linked to the modulation of protein synthesis in the infected host. “This is important because understanding the modulation of host protein synthesis by viruses can reveal how viruses manipulate the organism’s response to infection,” said lead author Dr Nicolas Locker, Lecturer in Virology.
"Noroviruses are a significant cause of gastroenteritis outbreaks worldwide - by understanding how these viruses control the host cell response to infection, we can identify ways to inhibit viral replication.”
Professor Lisa Roberts, senior author and Executive Dean of the Faculty of Health and Medical Sciences, said, “Our discovery proposes a new and alternative way of designing antiviral therapies by targeting cellular signalling events required for viral replication rather than trying to target the virus itself.”