About: HIV-1 mutates to evade IFITM1 restriction

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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	HIV-1 mutates to evade IFITM1 restriction
Creator	Ding, Shilei Liang, Chen Liu, Shan-Lu Pan, Qinghua
Source	Elsevier; Medline; PMC
abstract	Abstract Interferon-induced transmembrane (IFITM) proteins inhibit the infection of a wide range of viruses including human immunodeficiency virus type 1 (HIV-1). At present, little is known about how viruses overcome IFITM restriction. In this study, we have utilized HIV-1 as a model and selected IFITM1-resistant viruses after multiple passages of HIV-1 in IFITM1-expressing SupT1 cells. Sequencing the entire viral genome revealed several mutations in the vpu and envelope genes, among which mutations Vpu34 and EnvG367E together enable efficient HIV-1 replication in IFITM1-expressing cells. Vpu34 introduces a stop codon at amino acid position 35 of Vpu, whereas EnvG367E changes the G367 residue at the CD4-binding site of gp120. These two mutations do not appear to overcome the downregulation of viral p24 expression caused by IFITM1, but rather enhance HIV-1 replication by promoting cell-to-cell virus transmission. Altogether, our data demonstrate that HIV-1 can mutate to evade IFITM1 restriction by increasing cell-to-cell transmission.
has issue date	2014-04-30(xsd:dateTime)
bibo:doi	10.1016/j.virol.2014.01.020
bibo:pmid	24725927
has license	els-covid
sha1sum (hex)	ebc43d816d42000ef2dbae52769965bca0a27b33
schema:url	https://doi.org/10.1016/j.virol.2014.01.020
resource representing a document's title	HIV-1 mutates to evade IFITM1 restriction
has PubMed Central identifier	PMC4274668
has PubMed identifier	24725927
schema:publication	Virology
resource representing a document's body	covid:ebc43d816d42000ef2dbae52769965bca0a27b33#body_text
is schema:about of	named entity 'Vpu' named entity 'restriction' named entity 'proteins' covid:arg/ebc43d816d42000ef2dbae52769965bca0a27b33 named entity 'p24' named entity 'mutations' named entity 'position' named entity 'infection' named entity 'mutations' named entity 'data' named entity 'wide range' named entity 'cells' named entity 'HIV-1' named entity 'viruses' named entity 'HIV-1' named entity 'amino acid' named entity 'human immunodeficiency virus type 1' named entity 'HIV-1' named entity 'viruses' named entity 'infection' named entity 'viruses' named entity 'binding site' named entity 'HIV-1 genome' named entity 'coding region' named entity 'Western blotting' named entity 'IFITM1' named entity 'wild type' named entity 'SARS coronavirus' named entity 'HEK293T' named entity 'amino acids' named entity 'IFITM1' named entity 'IAV' named entity 'CD4' named entity 'highly conserved' named entity 'HCV' named entity 'genomic DNA' named entity 'apolipoprotein' named entity 'Invitrogen' named entity 'HIV-1' named entity 'BlaM' named entity 'viruses' named entity 'V3 loop' named entity 'wild type' named entity 'downregulate' named entity 'IFITM1' named entity 'IFITM1' named entity 'infection' named entity 'genome' named entity 'doxycycline' named entity 'protein' named entity 'antibody' named entity 'IFITM1' named entity 'AIDS' named entity 'wild type' named entity 'I-TASSER' named entity 'viral DNA' named entity 'Dengue virus' named entity 'start codon' named entity 'cytopathogenic effect' named entity 'Western blotting' named entity 'HIV-1' named entity 'mRNA' named entity 'protein' named entity 'infection' named entity 'enveloped viruses' named entity 'viruses' named entity 'HIV-1' named entity 'viruses' named entity 'infectivity' named entity 'lysed' named entity 'Env' named entity 'HIV-1' named entity 'infectivity' named entity 'RNase' named entity 'virion' named entity 'virus' named entity 'wild type' named entity 'infection'

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