TY - JOUR
T1 - When viruses collide
T2 - Hepatitis B virus reactivation after hepatitis C treatment
AU - Balagopal, Ashwin
AU - Thio, Chloe L.
N1 - Publisher Copyright:
© 2020, American Society for Clinical Investigation.
PY - 2020/6/1
Y1 - 2020/6/1
N2 - Treatment for hepatitis C virus (HCV) with direct-acting antivirals (DAAs) in hepatitis B virus (HBV) coinfection can result in HBV reactivation. In this issue of the JCI, Cheng and colleagues explored the role of interferon signaling in the complex interaction between HBV and HCV using cell lines, mouse models, and samples from people with coinfection. Notably, HCV enhanced interferon signaling, as measured by interferon-stimulated gene (ISG) expression, and decreased HBV transcription and replication. Blockade of interferon signaling reversed the effects on HBV replication. Further, pharmacologic inhibition of HCV replication in vitro and in coinfected humanized mice also reduced interferon signaling and, correspondingly, increased HBV replication. Intriguingly, baseline serum levels of the ISG CXCL10 predicted HBV reactivation in a cohort of coinfected people taking DAAs. Determining how interferon signaling silences HBV transcription and whether serum CXCL10 predicts HBV reactivation in a clinical setting are questions that warrant further investigation.
AB - Treatment for hepatitis C virus (HCV) with direct-acting antivirals (DAAs) in hepatitis B virus (HBV) coinfection can result in HBV reactivation. In this issue of the JCI, Cheng and colleagues explored the role of interferon signaling in the complex interaction between HBV and HCV using cell lines, mouse models, and samples from people with coinfection. Notably, HCV enhanced interferon signaling, as measured by interferon-stimulated gene (ISG) expression, and decreased HBV transcription and replication. Blockade of interferon signaling reversed the effects on HBV replication. Further, pharmacologic inhibition of HCV replication in vitro and in coinfected humanized mice also reduced interferon signaling and, correspondingly, increased HBV replication. Intriguingly, baseline serum levels of the ISG CXCL10 predicted HBV reactivation in a cohort of coinfected people taking DAAs. Determining how interferon signaling silences HBV transcription and whether serum CXCL10 predicts HBV reactivation in a clinical setting are questions that warrant further investigation.
UR - http://www.scopus.com/inward/record.url?scp=85085904579&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85085904579&partnerID=8YFLogxK
U2 - 10.1172/JCI137477
DO - 10.1172/JCI137477
M3 - Review article
C2 - 32420916
AN - SCOPUS:85085904579
SN - 0021-9738
VL - 130
SP - 2823
EP - 2826
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 6
ER -