Advances in the study of viruses inhibiting the production of advanced autophagy or interferon through Rubicon to achieve innate immune escape.
- Author:
Junwei SU
1
;
Jin YUAN
2
;
Feng WANG
3
;
Jun LI
3
;
Lei YUE
4
;
Min YAN
5
,
6
Author Information
1. Department of Pathogen Biology and Immunology, Kunming Medical University, Kunming 650500; Department of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou 310016, China.
2. Department of Clinical Laboratory, Puer Hospital of Traditional Chinese Medicine, Puer 665099, China.
3. Department of Pathogen Biology and Immunology, Kunming Medical University, Kunming 650500, China.
4. Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical Collge, Kunming 650118, China. *Corresponding authors, E-mail: lei_yue@outlook.com.
5. Department of Pathogen Biology and Immunology, Kunming Medical University, Kunming 650500, China. *Corresponding authors, E-mail: yanmin0310606@
6. com.
- Publication Type:English Abstract
- MeSH:
Humans;
Autophagy/immunology*;
Immunity, Innate;
Interferons/immunology*;
Immune Evasion;
Animals;
Virus Diseases/virology*;
Signal Transduction;
Viruses/immunology*;
Intracellular Signaling Peptides and Proteins/immunology*;
Autophagy-Related Proteins
- From:
Chinese Journal of Cellular and Molecular Immunology
2025;41(1):83-89
- CountryChina
- Language:Chinese
-
Abstract:
The innate immune response is the first line of defense for the host against viral infections. Targeted degradation of pathogenic microorganisms through autophagy, in conjunction with pattern recognition receptors synergistically inducing the production of interferon (IFN), constitutes an important pathway for the body to resist viral infections. Rubicon, a Run domain Beclin 1-interacting and cysteine-rich domain protein, has an inhibitory effect on autophagy and IFN production. On the one hand, Rubicon, as a component of the phosphoinositide 3-kinase (PI3K) complex, interacts with different domains of vacuolar protein sorting 34 (Vps34), ultraviolet radiation resistance associated gene (UVRAG), guanosine triphosphate (GTP) kinase, and RAS oncogene family member 7 (Rab7) to mediate the inhibition of autophagy maturation; on the other hand, Rubicon inhibits the ubiquitination of nuclear factor κB essential modulator (NEMO) and the dimerization of interferon regulatory factor 3 (IRF3), thereby blocking the signal transduction related to IFN production. Research has revealed that various viruses, such as Kaposi's sarcoma-associated herpesvirus (KSHV), hepatitis B virus (HBV), Sendai virus (SeV), and hepatitis C virus (HCV), achieve innate immune evasion by regulating the expression or function of Rubicon. Rubicon is expected to be a new target for antiviral therapy.
