期刊
VIRUSES-BASEL
卷 13, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/v13091819
关键词
HIV; tRNA; Gag; matrix; capsid; replication; reverse transcription
类别
资金
- Intramural Research Program of the NIH, The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [ZIADK075136]
- NIH Deputy Director for Intramural Research (DDIR) Challenge Award
The cellular metabolism of host tRNAs and the life cycle of HIV-1 intersect at various key interfaces, with the virus hijacking host tRNAs for reverse transcription and structural protein regulation, providing potential targets for the development of HIV/AIDS treatments.
The cellular metabolism of host tRNAs and life cycle of HIV-1 cross paths at several key virus-host interfaces. Emerging data suggest a multi-faceted interplay between host tRNAs and HIV-1 that plays essential roles, both structural and regulatory, in viral genome replication, genome packaging, and virion biogenesis. HIV-1 not only hijacks host tRNAs and transforms them into obligatory reverse transcription primers but further commandeers tRNAs to regulate the localization of its major structural protein, Gag, via a specific interface. This review highlights recent advances in understanding tRNA-HIV-1 interactions, primarily from a structural perspective, which start to elucidate their underlying molecular mechanisms, intrinsic specificities, and biological significances. Such understanding may provide new avenues toward developing HIV/AIDS treatments and therapeutics including small molecules and RNA biologics that target these host-virus interfaces.
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