期刊
CELLS
卷 10, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/cells10081864
关键词
TRIM22; DNA and RNA viruses; HIV-1; influenza A virus; interferons
类别
资金
- Ministry of Education, University and Research, Italy [2017TYTWZ3]
Upon viral invasion, host cells activate defense mechanisms to prevent further viral propagation through the production of type I interferons and activation of IFN-stimulated genes. TRIM22, as a member of the TRIM family, plays a crucial role in antiviral defense by targeting various DNA and RNA viruses, such as HIV-1 and IAV, through direct or indirect interactions with viral components at both protein and chromatin levels.
Viral invasion of target cells triggers an immediate intracellular host defense system aimed at preventing further propagation of the virus. Viral genomes or early products of viral replication are sensed by a number of pattern recognition receptors, leading to the synthesis and production of type I interferons (IFNs) that, in turn, activate a cascade of IFN-stimulated genes (ISGs) with antiviral functions. Among these, several members of the tripartite motif (TRIM) family are antiviral executors. This article will focus, in particular, on TRIM22 as an example of a multitarget antiviral member of the TRIM family. The antiviral activities of TRIM22 against different DNA and RNA viruses, particularly human immunodeficiency virus type 1 (HIV-1) and influenza A virus (IAV), will be discussed. TRIM22 restriction of virus replication can involve either direct interaction of TRIM22 E3 ubiquitin ligase activity with viral proteins, or indirect protein-protein interactions resulting in control of viral gene transcription, but also epigenetic effects exerted at the chromatin level.
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