Evidence map›Paper›PMID 35081977›Full record

ArticleRetrovirology2022

Bone marrow stromal antigen 2 (BST-2) genetic variants influence expression levels and disease outcome in HIV-1 chronically infected patients.

Hlelolwenkosi Mlimi, Kewreshini K Naidoo, Jenniffer Mabuka, Thumbi Ndung'u, Paradise Madlala

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Article in Retrovirology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Hlelolwenkosi MlimiHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, 719 Umbilo Road, Durban, 4013, South Africa.
Kewreshini K NaidooHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, 719 Umbilo Road, Durban, 4013, South Africa.
Jenniffer MabukaDepartment of Global Health, University of Washington, Seattle, USA.
Thumbi Ndung'uHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, 719 Umbilo Road, Durban, 4013, South Africa.
Paradise MadlalaHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, 719 Umbilo Road, Durban, 4013, South Africa. madlalap@ukzn.ac.za.ORCID 0000-0003-0641-1452
University of KwaZulu-Natal · ZARagon Institute of MGH, MIT and Harvard · USUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBone marrow stromal antigen 2 (BST-2) also known as Tetherin (CD317/HM1.24), is a host restriction factor that blocks the release of HIV-1 virions from infected cells. Previous studies reported that BST-2 genetic variants or single nucleotide polymorphims (SNPs) have a preventative role during HIV-1 infection. However, the influence of BST-2 SNPs on expression levels remains unknown. In this study, we investigated the influence of BST-2 SNPs on expression levels and disease outcome in HIV-1 subtype C chronically infected antiretroviral therapy naïve individuals.

resultsWe quantified BST-2 mRNA levels in peripheral blood mononuclear cells (PBMCs), determined BST-2 protein expression on the surface of CD4

conclusionOur findings show that bst-2 SNPs mediate BST-2 expression and disease outcome, correlate with gp120-IgG1, gp120-IgG3 levels but not p24-IgG levels, ADCC and ADCP activity.

Indexed as

HIV-1HIV InfectionsAntibody-Dependent Cell CytotoxicityAntigens, CDBone Marrow Stromal Antigen 2CD4-Positive T-LymphocytesGPI-Linked ProteinsHIV Envelope Protein gp120HumansImmunoglobulin GLeukocytes, MononuclearRNA, MessengerAntigens, CDBone Marrow Stromal Antigen 2BST2 protein, humanGPI-Linked ProteinsHIV Envelope Protein gp120Immunoglobulin GRNA, MessengerBST-2Expression levelsgp120- and p24-IgG levelsSNPsViral loads

Identifiers

PMID35081977
PMCPMC8793201
OpenAlexW4226120243

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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.