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Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma

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Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma. / Chen, Jingyan; Tibroni, Nadine; Sauter, Daniel; Galaski, Johanna; Miura, Toshiyuki; Alter, Galit; Mueller, Birthe; Haller, Claudia; Walker, Bruce D; Kirchhoff, Frank; Brumme, Zabrina L; Ueno, Takamasa; Fackler, Oliver T.

In: PLOS ONE, Vol. 10, No. 3, 2015, p. e0120434.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Chen, J, Tibroni, N, Sauter, D, Galaski, J, Miura, T, Alter, G, Mueller, B, Haller, C, Walker, BD, Kirchhoff, F, Brumme, ZL, Ueno, T & Fackler, OT 2015, 'Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma', PLOS ONE, vol. 10, no. 3, pp. e0120434. https://doi.org/10.1371/journal.pone.0120434

APA

Chen, J., Tibroni, N., Sauter, D., Galaski, J., Miura, T., Alter, G., Mueller, B., Haller, C., Walker, B. D., Kirchhoff, F., Brumme, Z. L., Ueno, T., & Fackler, O. T. (2015). Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma. PLOS ONE, 10(3), e0120434. https://doi.org/10.1371/journal.pone.0120434

Vancouver

Chen J, Tibroni N, Sauter D, Galaski J, Miura T, Alter G et al. Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma. PLOS ONE. 2015;10(3):e0120434. https://doi.org/10.1371/journal.pone.0120434

Bibtex

@article{af964217b11c4be498e676e6dd2bc756,
title = "Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma",
abstract = "In the absence of antiretroviral therapy, infection with human immunodeficiency virus type 1 (HIV-1) can typically not be controlled by the infected host and results in the development of acquired immunodeficiency. In rare cases, however, patients spontaneously control HIV-1 replication. Mechanisms by which such elite controllers (ECs) achieve control of HIV-1 replication include particularly efficient immune responses as well as reduced fitness of the specific virus strains. To address whether polymorphisms in the accessory HIV-1 protein Vpu are associated with EC status we functionally analyzed a panel of plasma-derived vpu alleles from 15 EC and 16 chronic progressor (CP) patients. Antagonism of the HIV particle release restriction by the intrinsic immunity factor CD317/tetherin was well conserved among EC and CP Vpu alleles, underscoring the selective advantage of this Vpu function in HIV-1 infected individuals. In contrast, interference with CD317/tetherin induced NF-κB activation was little conserved in both groups. EC Vpus more frequently displayed reduced ability to downregulate cell surface levels of CD4 and MHC class I (MHC-I) molecules as well as of the NK cell ligand NTB-A. Polymorphisms potentially associated with high affinity interactions of the inhibitory killer immunoglobulin-like receptor (KIR) KIR2DL2 were significantly enriched among EC Vpus but did not account for these functional differences. Together these results suggest that in a subgroup of EC patients, some Vpu functions are modestly reduced, possibly as a result of host selection.",
keywords = "Alleles, Amino Acid Sequence, CD4 Antigens, Cell Membrane, Conserved Sequence, Disease Progression, Down-Regulation, Green Fluorescent Proteins, HEK293 Cells, HIV Infections, HIV-1, Histocompatibility Antigens Class I, Human Immunodeficiency Virus Proteins, Humans, Likelihood Functions, Molecular Sequence Data, NF-kappa B, Phylogeny, RNA, Viral, Sequence Analysis, Protein, Signal Transduction, Viral Regulatory and Accessory Proteins, Journal Article, Research Support, Non-U.S. Gov't",
author = "Jingyan Chen and Nadine Tibroni and Daniel Sauter and Johanna Galaski and Toshiyuki Miura and Galit Alter and Birthe Mueller and Claudia Haller and Walker, {Bruce D} and Frank Kirchhoff and Brumme, {Zabrina L} and Takamasa Ueno and Fackler, {Oliver T}",
year = "2015",
doi = "10.1371/journal.pone.0120434",
language = "English",
volume = "10",
pages = "e0120434",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "3",

}

RIS

TY - JOUR

T1 - Modest attenuation of HIV-1 Vpu alleles derived from elite controller plasma

AU - Chen, Jingyan

AU - Tibroni, Nadine

AU - Sauter, Daniel

AU - Galaski, Johanna

AU - Miura, Toshiyuki

AU - Alter, Galit

AU - Mueller, Birthe

AU - Haller, Claudia

AU - Walker, Bruce D

AU - Kirchhoff, Frank

AU - Brumme, Zabrina L

AU - Ueno, Takamasa

AU - Fackler, Oliver T

PY - 2015

Y1 - 2015

N2 - In the absence of antiretroviral therapy, infection with human immunodeficiency virus type 1 (HIV-1) can typically not be controlled by the infected host and results in the development of acquired immunodeficiency. In rare cases, however, patients spontaneously control HIV-1 replication. Mechanisms by which such elite controllers (ECs) achieve control of HIV-1 replication include particularly efficient immune responses as well as reduced fitness of the specific virus strains. To address whether polymorphisms in the accessory HIV-1 protein Vpu are associated with EC status we functionally analyzed a panel of plasma-derived vpu alleles from 15 EC and 16 chronic progressor (CP) patients. Antagonism of the HIV particle release restriction by the intrinsic immunity factor CD317/tetherin was well conserved among EC and CP Vpu alleles, underscoring the selective advantage of this Vpu function in HIV-1 infected individuals. In contrast, interference with CD317/tetherin induced NF-κB activation was little conserved in both groups. EC Vpus more frequently displayed reduced ability to downregulate cell surface levels of CD4 and MHC class I (MHC-I) molecules as well as of the NK cell ligand NTB-A. Polymorphisms potentially associated with high affinity interactions of the inhibitory killer immunoglobulin-like receptor (KIR) KIR2DL2 were significantly enriched among EC Vpus but did not account for these functional differences. Together these results suggest that in a subgroup of EC patients, some Vpu functions are modestly reduced, possibly as a result of host selection.

AB - In the absence of antiretroviral therapy, infection with human immunodeficiency virus type 1 (HIV-1) can typically not be controlled by the infected host and results in the development of acquired immunodeficiency. In rare cases, however, patients spontaneously control HIV-1 replication. Mechanisms by which such elite controllers (ECs) achieve control of HIV-1 replication include particularly efficient immune responses as well as reduced fitness of the specific virus strains. To address whether polymorphisms in the accessory HIV-1 protein Vpu are associated with EC status we functionally analyzed a panel of plasma-derived vpu alleles from 15 EC and 16 chronic progressor (CP) patients. Antagonism of the HIV particle release restriction by the intrinsic immunity factor CD317/tetherin was well conserved among EC and CP Vpu alleles, underscoring the selective advantage of this Vpu function in HIV-1 infected individuals. In contrast, interference with CD317/tetherin induced NF-κB activation was little conserved in both groups. EC Vpus more frequently displayed reduced ability to downregulate cell surface levels of CD4 and MHC class I (MHC-I) molecules as well as of the NK cell ligand NTB-A. Polymorphisms potentially associated with high affinity interactions of the inhibitory killer immunoglobulin-like receptor (KIR) KIR2DL2 were significantly enriched among EC Vpus but did not account for these functional differences. Together these results suggest that in a subgroup of EC patients, some Vpu functions are modestly reduced, possibly as a result of host selection.

KW - Alleles

KW - Amino Acid Sequence

KW - CD4 Antigens

KW - Cell Membrane

KW - Conserved Sequence

KW - Disease Progression

KW - Down-Regulation

KW - Green Fluorescent Proteins

KW - HEK293 Cells

KW - HIV Infections

KW - HIV-1

KW - Histocompatibility Antigens Class I

KW - Human Immunodeficiency Virus Proteins

KW - Humans

KW - Likelihood Functions

KW - Molecular Sequence Data

KW - NF-kappa B

KW - Phylogeny

KW - RNA, Viral

KW - Sequence Analysis, Protein

KW - Signal Transduction

KW - Viral Regulatory and Accessory Proteins

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1371/journal.pone.0120434

DO - 10.1371/journal.pone.0120434

M3 - SCORING: Journal article

C2 - 25793728

VL - 10

SP - e0120434

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 3

ER -