Interferons are released by virally-infected cells, serving as messengers to surrounding cells that a viral infection is nigh. Some interferons can trigger apoptosis in lost cells already infected to prevent the virus from reaching more healthy cells, and they are also responsible for mounting a larger immune response targeting the invader.
"The finding helps explain why many patients fail [to respond to] certain drug treatments, and should help develop more effective alternate treatment protocols," said corresponding author of recent University of Washington study, Ram Savan, PhD.
A previous study from Savan’s group looked at hepatitis C virus invading a liver cell. The virus takes over the use of the host cell’s cellular machinery, triggering the activation of two genes, MYH7 and MYH7B, that produce two microRNAs that interfere with the production of two interferons. They also found that the same microRNAs inhibit the production of a critical receptor for the interferon-driven antiviral immune response.
With a dual, virus-driven attack on interferon production, hepatitis C-infected cells are left virtually defenseless and unable to warn their peers of an imminent attack.
"This may in part explain why interferon treatments, which harness a type I interferon, fail in so many patients," said lead author and current graduate student Abigail Jarret.
Jarret’s current study was published recently in the journal Nature Medicine.
Source: University of Washington Health Sciences/UW Medicine