© Dr. Caroline Lilley/Salk Institute for Biological Studies
When cells with DNA damage are infected with HSV-1 virus (top image, virus shown in red) the viral ICP0 protein prevents the DNA repair proteins (bottom image, DNA repair proteins shown in green) from accumulating at sites of DNA damage.
A viral infection is like an uninvited, tenacious houseguest in the cell, using a range of tricks to prevent its eviction. Researchers at the Salk Institute for Biological Studies have identified one of the key proteins allowing herpes simplex virus (HSV) DNA to fly under the radar of their hosts' involuntary hospitality.
Their findings, to be published in a forthcoming issue of
The EMBO Journal, reveal one of the tactics that HSV employs in order to overcome its hosts' defenses and may suggest a common mechanism by which viruses can successfully infect host cells.
HSV, like all viruses, requires a living host in order to multiply. But before it can hijack the cellular machinery to produce scores of copies of itself, it needs to evade the cell's security system. "We found that detection of the viral DNA by the host cell is an important barrier that the virus must overcome in order to achieve its goal," says Matthew Weitzman, Ph.D., associate professor in the Laboratory of Genetics, who led the study. "For this purpose, it brings along a protein that shuts down the normal cellular responses that would otherwise recognize and silence it."
To the host cell, invading viral DNA looks just like the product of DNA damage, which must be repaired or removed in order for the cell to stay healthy. As a result, DNA "security guards" continuously patrol our cells looking for unusual bits of DNA. "We reasoned that viral DNA would be recognized by the cell's DNA repair machinery and that the virus must somehow manipulate the cell's response to this foreign DNA," explains Weitzman.
