Related Experiment Videos
Inducible Rubicon facilitates viral replication by antagonizing interferon production
Yushun Wan1, Wei Cao1, Tao Han1
1State Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, China.
Cellular & Molecular Immunology
|April 11, 2017
Summary
Rubicon protein enhances viral replication by inhibiting interferon production. This study reveals Rubicon
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Rubicon protein regulates autophagy and endocytic pathways.
- Its role in viral infections and interferon signaling remains unclear.
Purpose of the Study:
- To investigate Rubicon's function in viral resistance to interferon (IFN).
- To elucidate Rubicon's mechanism in viral immune evasion.
Main Methods:
- Assessed Rubicon protein levels in hepatitis B virus (HBV) infected patients.
- Performed Rubicon overexpression and knockdown assays.
- Investigated Rubicon's interaction with NEMO and IRF3/IRF7 translocation.
Main Results:
- Rubicon levels are elevated in HBV infection.
- Rubicon promotes HBV replication and inhibits other viruses (enterovirus 71, influenza A, VSV).
- Rubicon suppresses type-I and type-III interferon production by interacting with NEMO, inhibiting IRF3/IRF7 nuclear translocation.
Conclusions:
- Rubicon is a virus-induced protein that inhibits innate immune response by suppressing interferon production.
- Rubicon enhances viral replication and contributes to viral immune evasion.