About: Interferon-induced HERC5 is evolving under positive selection and inhibits HIV-1 particle production by a novel mechanism targeting Rev/RRE-dependent RNA nuclear export

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About: Interferon-induced HERC5 is evolving under positive selection and inhibits HIV-1 particle production by a novel mechanism targeting Rev/RRE-dependent RNA nuclear export Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Interferon-induced HERC5 is evolving under positive selection and inhibits HIV-1 particle production by a novel mechanism targeting Rev/RRE-dependent RNA nuclear export
Creator	Barr, Stephen Cavanagh, Craig Dikeakos, Jimmy Szabo, Peter Tom, Sean Tong, Jessica Woods, Matthew
source	Medline; PMC
abstract	BACKGROUND: Type I interferon (IFN) inhibits virus replication by activating multiple antiviral mechanisms and pathways. It has long been recognized that type I IFNs can potently block HIV-1 replication in vitro; as such, HIV-1 has been used as a system to identify and characterize IFN-induced antiviral proteins responsible for this block. IFN-induced HERC5 contains an amino-terminal Regulator of Chromosome Condensation 1 (RCC1)-like domain and a carboxyl-terminal Homologous to the E6-AP Carboxyl Terminus (HECT) domain. HERC5 is the main cellular E3 ligase that conjugates the IFN-induced protein ISG15 to proteins. This E3 ligase activity was previously shown to inhibit the replication of evolutionarily diverse viruses, including HIV-1. The contribution of the RCC1-like domain to the antiviral activity of HERC5 was previously unknown. RESULTS: In this study, we showed that HERC5 inhibits HIV-1 particle production by a second distinct mechanism that targets the nuclear export of Rev/RRE-dependent RNA. Unexpectedly, the E3 ligase activity of HERC5 was not required for this inhibition. Instead, this activity required the amino-terminal RCC1-like domain of HERC5. Inhibition correlated with a reduction in intracellular RanGTP protein levels and/or the ability of RanGTP to interact with RanBP1. Inhibition also correlated with altered subcellular localization of HIV-1 Rev. In addition, we demonstrated that positive evolutionary selection is operating on HERC5. We identified a region in the RCC1-like domain that exhibits an exceptionally high probability of having evolved under positive selection and showed that this region is required for HERC5-mediated inhibition of nuclear export. CONCLUSIONS: We have identified a second distinct mechanism by which HERC5 inhibits HIV-1 replication and demonstrate that HERC5 is evolving under strong positive selection. Together, our findings contribute to a growing body of evidence suggesting that HERC5 is a novel host restriction factor.
has issue date	2014-04-03(xsd:dateTime)
bibo:doi	10.1186/1742-4690-11-27
bibo:pmid	24693865
has license	cc-by
sha1sum (hex)	d65ef4b00759d797d28454625b4de2814675bb56
schema:url	https://doi.org/10.1186/1742-4690-11-27
resource representing a document's title	Interferon-induced HERC5 is evolving under positive selection and inhibits HIV-1 particle production by a novel mechanism targeting Rev/RRE-dependent RNA nuclear export
has PubMed Central identifier	PMC4021598
has PubMed identifier	24693865
schema:publication	Retrovirology
resource representing a document's body	covid:d65ef4b00759d797d28454625b4de2814675bb56#body_text
is schema:about of	named entity 'PROTEINS' named entity 'CONTAINS' named entity 'LIGASE ACTIVITY' named entity 'TO INHIBIT' named entity 'INDUCED' named entity 'MULTIPLE' named entity 'MECHANISMS' named entity 'PREVIOUSLY' named entity 'MAIN' named entity 'VIRUS REPLICATION' named entity 'TO IDENTIFY' named entity 'HOMOLOGOUS' named entity 'REPLICATION' named entity 'TERMINUS' named entity 'PARTICLE' named entity 'protein' named entity 'antiviral' named entity 'targeting' covid:arg/d65ef4b00759d797d28454625b4de2814675bb56 named entity 'IN VITRO' named entity 'AMINO' named entity 'PATHWAYS' named entity 'USED' named entity 'CARBOXYL' named entity 'HIV-1' named entity 'HERC5' named entity 'RESPONSIBLE' named entity 'INTERFERON ' named entity 'TYPE I INTERFERON' named entity 'TYPE I' named entity 'DOMAIN' named entity 'CONJUGATES' named entity 'HERC5' named entity 'NUCLEAR EXPORT' named entity 'INTERFERON' named entity 'EVOLVING' named entity 'INDUCED' named entity 'DEPENDENT' named entity 'RNA' named entity 'NOVEL' named entity 'TARGETING' named entity 'HIV-1' named entity 'HIV-1 REPLICATION' named entity 'INCLUDING' named entity 'UNKNOWN' named entity 'VIRUSES' named entity 'ANTIVIRAL' named entity 'CONTRIBUTION' named entity 'E6-AP' named entity 'LIKE' named entity 'REGULATOR OF CHROMOSOME CONDENSATION 1' named entity 'REV' named entity 'MECHANISM' named entity 'POSITIVE SELECTION' named entity 'PRODUCTION' named entity 'DIVERSE' named entity 'ISG15' named entity 'RCC1-LIKE' named entity 'LONG' named entity 'ANTIVIRAL ACTIVITY' named entity 'CELLULAR' named entity 'BLOCK' named entity 'IFN' named entity 'ACTIVATING' named entity 'LIGASE' named entity 'BACKGROUND' named entity 'TERMINAL' named entity 'SYSTEM' named entity 'PROTEIN ' named entity 'conjugates' named entity 'Condensation' named entity 'activity' named entity 'Terminus' named entity 'Carboxyl' named entity 'activity'

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