A recent letter in Nature
Medicine has shed some more light on Hepatitis C virus’ impact on the
immune system of compromised individuals. The research team, led by Abigail
Jarret, a graduate student at Yale University, reported that two microRNAs, miR-208b
and miR-499a-5p, which are overexpressed in infected hepatocytes, weaken immune
response through downregulating IFNAR1 (a type I interferon receptor) expression.
Previous studies have shown that miR-208b and miR-499a-5p also suppress
expression of IFNL2 and IFNL3, both type III interferons, thus increasing HCV persistence.
This work helps to explain why current interferon-alpha and ribavirin
therapies are not as effective as researchers would hope. We now know that HCV
impacts the immune response in two ways – by halting type III interferon assembly,
and by preventing production of the receptors type I interferons need to properly
function. According to Jarret, since these therapies utilize type I interferon,
HCV may be able to persist by simply inactivating type III interferons, explaining
why treatment fails for nearly 60% of patients.
Ahmed Mustafa
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