About the Project
Infections come in all shapes and sizes, and over the history of our species, have killed more human beings than anything else. About 15 million people die each year of infectious diseases such as respiratory infection, HIV/AIDS, diarrheal diseases, tuberculosis, malaria, hepatitis B and C viruses. Emerging viral infection including SARS, H7N9, Ebola, and Zika viruses broke out almost every year in the past decade. Human innate and adaptive immune responses are essential to defense pathogen infections and control infectious diseases, during which rapid and robust production of interferon (IFN) is a critical event. Particularly, type I IFN play important roles in host antiviral immune responses. Long noncoding RNAs (lncRNAs) have been shown to play important roles in immune cell development and immune responses through different mechanisms, such as dosage compensation, imprinting, enhancer function, and transcriptional regulation. Although the functions of most lncRNAs are unclear, some lncRNAs have been found to control transcriptional or post-transcriptional regulation of the innate and adaptive immune responses via new methods of protein–protein interactions or pairing with DNA and RNA. Interestingly, increasing evidence has supported the important roles of lncRNAs in the interaction between hosts and pathogens in a type I IFN-dependent or independent pathways. N6-methyladenosine (m6A) modification in mRNA is extremely widespread, and functionally modulates the eukaryotic transcriptome to influence mRNA splicing, export, localization, translation, and stability. Methylated adenines are also present in a large subset of mRNAs and lncRNAs in resting and activated immune cells. The protein factors involved in m6A modification system consist of: the m6A ‘writer’, which methylates the adenosine at the N6 position; ‘erasers’, which catalyze the reversible oxidative demethylation of the methyl group from m6A; and ‘readers’, a group of effector components that determine the fate of modified mRNAs by binding to m6A. These three factors collectively orchestrate the m6A RNA methylome in the eukaryotic cell. Upon viral infection, the expression profiles of lncRNA in host cells are affected dramatically. In addition, the m6A modification is also changed in multiple mRNAs and lncRNAs during host cells fight against invading viruses, which potentially controls host antiviral immunity.
References
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