Identification of novel Mechanism for Viral Immune Escape and Replication by Xuetao Cao's research Group
Source：Pin Wang
2017-12-27
After publishing the Perspective on intestinal bacteria inflammation in Science last month, a new research paper from Cao's lab was published in Science on November 24, 2017. They found a viral-induced lncRNA-ACOD1 was able to promote viral immune escape and replication through regulating metabolic status of host cells. This finding provided new insights into viral replication and a potential target for developing broad-acting antiviral drugs and therapeutics.
How viruses change the host cells in order to escape from immune clearance has always been a vital question in the study of immunology and virology. Interferons are key factors defending virus infection，but how viruses escape from clearance is still elusive. In this work supported by grants from the National Natural Science Foundation of China, CAMS Innovation Fund for Medical Sciences, and Shanghai Rising-Star Program, Xuetao Cao and associate professor Pin Wang from the State Key Laboratory of Medical Immunology, PhD students Junfang Xu and Yujia Wang from Institute of Immunology at Zhejiang University worked together to screen highly expressed lncRNAs in the macrophages after viral infection，identifying a group of viral-induced, IFN-I-independent lncRNAs. One of them named lncRNA-ACOD1 can significantly promote replicationof different viruses through directly binding to the metabolic enzyme glutamic-oxaloacetic transaminase 2 (GOT2) and modulating host metabolism.
This work proposed a new perspective on how viruses hijack host metabolism for their own survival through an uncovered new regulatory networks between epigenetics, cell metabolism and viral infection, putting forward a new research direction of lncRNA in the interaction between virus and host.
How viruses change the host cells in order to escape from immune clearance has always been a vital question in the study of immunology and virology. Interferons are key factors defending virus infection，but how viruses escape from clearance is still elusive. In this work supported by grants from the National Natural Science Foundation of China, CAMS Innovation Fund for Medical Sciences, and Shanghai Rising-Star Program, Xuetao Cao and associate professor Pin Wang from the State Key Laboratory of Medical Immunology, PhD students Junfang Xu and Yujia Wang from Institute of Immunology at Zhejiang University worked together to screen highly expressed lncRNAs in the macrophages after viral infection，identifying a group of viral-induced, IFN-I-independent lncRNAs. One of them named lncRNA-ACOD1 can significantly promote replicationof different viruses through directly binding to the metabolic enzyme glutamic-oxaloacetic transaminase 2 (GOT2) and modulating host metabolism.
This work proposed a new perspective on how viruses hijack host metabolism for their own survival through an uncovered new regulatory networks between epigenetics, cell metabolism and viral infection, putting forward a new research direction of lncRNA in the interaction between virus and host.
