Nef-mediated inhibition of NFAT following TCR stimulation differs between HIV-1 subtypes.
HIV-1 Nef
HIV-1 disease progression
HIV-1 subtype C
HLA-associated polymorphisms
Immune-driven escape mutations
NFAT inhibition
TCR signalling
Journal
Virology
ISSN: 1096-0341
Titre abrégé: Virology
Pays: United States
ID NLM: 0110674
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
13
12
2018
revised:
13
02
2019
accepted:
16
02
2019
pubmed:
31
3
2019
medline:
23
10
2019
entrez:
31
3
2019
Statut:
ppublish
Résumé
Functional characterisation of different HIV-1 subtypes may improve understanding of viral pathogenesis and spread. Here, we evaluated the ability of 345 unique HIV-1 Nef clones representing subtypes A, B, C and D to inhibit NFAT signalling following TCR stimulation. The contribution of this Nef function to disease progression was also assessed in 211 additional Nef clones isolated from unique subtype C infected individuals in early or chronic infection. On average, subtype A and C Nef clones exhibited significantly lower ability to inhibit TCR-mediated NFAT signalling compared to subtype B and D Nef clones. While this observation corroborates accumulating evidence supporting relative attenuation of subtypes A and C that may paradoxically contribute to their increased global prevalence and spread, no significant correlations between Nef-mediated NFAT inhibition activity and clinical markers of HIV-1 infection were observed, indicating that the relationship between Nef function and pathogenesis is complex.
Identifiants
pubmed: 30927712
pii: S0042-6822(19)30057-1
doi: 10.1016/j.virol.2019.02.011
pmc: PMC6526282
mid: NIHMS1525613
pii:
doi:
Substances chimiques
NFATC Transcription Factors
0
Receptors, Antigen, T-Cell
0
nef Gene Products, Human Immunodeficiency Virus
0
nef protein, Human immunodeficiency virus 1
0
Types de publication
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
192-202Subventions
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NIAID NIH HHS
ID : R37 AI067073
Pays : United States
Organisme : NIAID NIH HHS
ID : UM1 AI126617
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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