About: IFITM Proteins Inhibit Entry Driven by the MERS-Coronavirus Spike Protein: Evidence for Cholesterol-Independent Mechanisms

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About: IFITM Proteins Inhibit Entry Driven by the MERS-Coronavirus Spike Protein: Evidence for Cholesterol-Independent Mechanisms Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	IFITM Proteins Inhibit Entry Driven by the MERS-Coronavirus Spike Protein: Evidence for Cholesterol-Independent Mechanisms
Creator	Pöhlmann, Stefan Winkler, Michael Wrensch, Florian
Source	Medline; PMC
abstract	The interferon-inducible transmembrane (IFITM) proteins 1, 2 and 3 inhibit the host cell entry of several enveloped viruses, potentially by promoting the accumulation of cholesterol in endosomal compartments. IFITM3 is essential for control of influenza virus infection in mice and humans. In contrast, the role of IFITM proteins in coronavirus infection is less well defined. Employing a retroviral vector system for analysis of coronavirus entry, we investigated the susceptibility of human-adapted and emerging coronaviruses to inhibition by IFITM proteins. We found that entry of the recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV) is sensitive to inhibition by IFITM proteins. In 293T cells, IFITM-mediated inhibition of cellular entry of the emerging MERS- and SARS-CoV was less efficient than blockade of entry of the globally circulating human coronaviruses 229E and NL63. Similar differences were not observed in A549 cells, suggesting that cellular context and/or IFITM expression levels can impact inhibition efficiency. The differential IFITM-sensitivity of coronaviruses observed in 293T cells afforded the opportunity to investigate whether efficiency of entry inhibition by IFITMs and endosomal cholesterol accumulation correlate. No such correlation was observed. Furthermore, entry mediated by the influenza virus hemagglutinin was robustly inhibited by IFITM3 but was insensitive to accumulation of endosomal cholesterol, indicating that modulation of cholesterol synthesis/transport did not account for the antiviral activity of IFITM3. Collectively, these results show that the emerging MERS-CoV is a target of the antiviral activity of IFITM proteins and demonstrate that mechanisms other than accumulation of endosomal cholesterol can contribute to viral entry inhibition by IFITMs.
has issue date	2014-09-26(xsd:dateTime)
bibo:doi	10.3390/v6093683
bibo:pmid	25256397
has license	cc-by
sha1sum (hex)	2fd379bd7d8ce15f444b2fa608e6c5899441d52a
schema:url	https://doi.org/10.3390/v6093683
resource representing a document's title	IFITM Proteins Inhibit Entry Driven by the MERS-Coronavirus Spike Protein: Evidence for Cholesterol-Independent Mechanisms
has PubMed Central identifier	PMC4189045
has PubMed identifier	25256397
schema:publication	Viruses
resource representing a document's body	covid:2fd379bd7d8ce15f444b2fa608e6c5899441d52a#body_text
is schema:about of	named entity 'emerging' named entity 'correlate' named entity 'MERS-CoV' named entity 'inhibition' named entity 'inhibition' named entity 'impact' named entity 'A549' named entity 'proteins' named entity 'antiviral' named entity 'Driven' named entity 'INDEPENDENT' named entity 'CORONAVIRUS INFECTION' named entity 'MECHANISMS' named entity 'CORRELATION' named entity 'ENTRY' named entity 'LEVELS' named entity 'HEMAGGLUTININ' named entity 'ENTRY' named entity 'OPPORTUNITY' named entity 'MIDDLE EAST RESPIRATORY SYNDROME CORONAVIRUS' named entity 'CONTRAST' named entity 'ESSENTIAL' covid:arg/2fd379bd7d8ce15f444b2fa608e6c5899441d52a named entity 'TRANSMEMBRANE' named entity 'MODULATION' named entity 'OBSERVED' named entity 'TARGET' named entity 'INTERFERON' named entity 'RECENTLY' named entity 'INDUCIBLE' named entity 'IS A' named entity 'ROLE' named entity 'VIRUSES' named entity 'BUT' named entity 'DRIVEN' named entity 'PROTEINS' named entity 'CHOLESTEROL' named entity 'SPIKE PROTEIN' named entity 'CIRCULATING' named entity 'A549 CELLS' named entity 'ACCOUNT' named entity 'INHIBITED' named entity 'MEDIATED' named entity 'ADAPTED' named entity 'EXPRESSION' named entity 'THESE' named entity 'CORONAVIRUSES' named entity 'INDICATING' named entity 'SENSITIVITY' named entity 'FOUND' named entity 'CORONAVIRUS' named entity 'MERS' named entity 'NOT OBSERVED' named entity 'INVESTIGATED' named entity 'ANALYSIS' named entity 'INSENSITIVE' named entity '293T CELLS' named entity 'HUMANS' named entity 'VIRUS INFECTION' named entity 'ACCUMULATION' named entity 'RETROVIRAL VECTOR' named entity 'SIMILAR' named entity 'CONTROL' named entity 'CHOLESTEROL SYNTHESIS' named entity 'INHIBITION' named entity 'SYSTEM' named entity 'PROMOTING' named entity 'COMPARTMENTS' named entity 'NL63' named entity 'EFFICIENT' named entity 'GLOBALLY' named entity 'TO INVESTIGATE' named entity 'HUMAN' named entity 'SENSITIVE TO' named entity 'CORONAVIRUS' named entity 'MERS' named entity 'CELLULAR' named entity 'ANTIVIRAL ACTIVITY' named entity 'BLOCKADE'

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