Simian-Human immunodeficiency viruses expressing chimeric subtype B/C Vpu proteins demonstrate the importance of the amino terminal and transmembrane domains in the rate of CD4(+) T cell loss in macaques.

Autumn Ruiz, Kimberly Schmitt, Nathan Culley, Edward B Stephens

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Article in Virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it

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3citing papers in PubMed

0.3field-weighted citation impact, top 45% of its field

1 · What the graph read from it

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

The Envelope Cytoplasmic Tail of HIV-1 Subtype C Contributes to Poor Replication Capacity through Low Viral Infectivity and Cell-to-Cell Transmission.PloS one · 2016
Article
Involvement of a C-terminal motif in the interference of primate lentiviral Vpu proteins with CD1d-mediated antigen presentation.Scientific reports · 2015
Article
A comparative mutational analysis of HIV-1 Vpu subtypes B and C for the identification of determinants required to counteract BST-2/Tetherin and enhance viral egress.Virology · 2013
Article

4 · The record

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5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Autumn RuizDepartment of Microbiology, Molecular Genetics, and Immunology, University of Kansas Medical Center, Kansas City, KS 66160, USA.

Kimberly Schmitt

Nathan Culley

Edward B Stephens

University of Kansas Medical Center · US

Funding

THE ROLE OF VPU IN HIV-1 PATHOGENESISR01AI051981 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI STEPHENS, EDWARD BRICE · 2002 to 2011

$3.1M

NIAID NIH HHS AI51981NIAID NIH HHS R01 AI051981

6 · The paper itself

Abstract

Previously, we reported that simian-human immunodeficiency viruses expressing either the lab adapted subtype B (SHIV(KU-1bMC33)) or subtype C (SHIV(SCVpu)) Vpu proteins of human immunodeficiency virus type 1 (HIV-1) had different rates of CD4(+) T cell loss following inoculation into macaques. In this study, we have generated SHIVs that express either the subtype B or subtype C N-terminal (NTD) and transmembrane (TMD) domains and the opposing cytoplasmic domain (SHIV(VpuBC), SHIV(VpuCB)). In culture systems, SHIV(VpuBC) replicated faster than SHIV(VpuCB) while both proteins exhibited similar ability to down-modulate CD4 surface expression. Following inoculation into macaques, SHIV(VpuBC) resulted in rapid CD4(+) T cell loss similar to the parental SHIV(KU-1bMC33), while the rate of CD4(+) T cell loss in those inoculated with SHIV(VpuCB) was intermediate of SHIV(SCVpu) and SHIV(KU-1bMC33). These results emphasize the importance of the Vpu NTD/TMD region in the rate of CD4(+) T cell loss in the pathogenic X4 SHIV/macaque model.

Indexed as

Acquired Immunodeficiency SyndromeAnimalsCD4 Lymphocyte CountCD4-Positive T-LymphocytesCell LineDisease Models, AnimalGreen Fluorescent ProteinsHIV-1Human Immunodeficiency Virus ProteinsHumansMacaca nemestrinaRecombinant Fusion ProteinsSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusViral Regulatory and Accessory ProteinsViroporin Proteinsenhanced green fluorescent proteinGreen Fluorescent ProteinsHuman Immunodeficiency Virus ProteinsRecombinant Fusion ProteinsViral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1

Identifiers

PMID23218949

DOI10.1016/j.virol.2012.10.030

PMCPMC4104993

OpenAlexW2067368806

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.