Journal
NATURE MEDICINE
Volume 19, Issue 7, Pages 879-888Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3253
Keywords
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Funding
- NIAID NIH HHS [U19 AI088778, R56 AI060389, AI060389, AI88778, R01 AI060389] Funding Source: Medline
- NIDA NIH HHS [R01 DA024563, DA024563] Funding Source: Medline
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Hepatitis C virus (HCV) is a global public health problem involving chronic infection of the liver, which can cause liver disease and is linked with liver cancer. Viral innate immune evasion strategies and human genetic determinants underlie the transition of acute HCV infection to viral persistence and the support of chronic infection. Host genetic factors, such as sequence polymorphisms in IFNL3, a gene in the host interferon system, can influence both the outcome of the infection and the response to antiviral therapy. Recent insights into how HCV regulates innate immune signaling within the liver reveal a complex interaction of patient genetic background with viral and host factors of innate immune triggering and control that imparts the outcome of HCV infection and immunity.
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