Evidence map›Paper›PMID 27473095›Full record

ArticleBMC microbiology2016

Alpha-1-antitrypsin interacts with gp41 to block HIV-1 entry into CD4+ T lymphocytes.

Xueyuan Zhou, Zhu Liu, Jun Zhang, Joseph W Adelsberger, Jun Yang, Gregory F Burton

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Peptide and peptide-based inhibitors of SARS-CoV-2 entry.Advanced drug delivery reviews · 2020
    Review
  14. Neutrophil Modulation in Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020
    Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Xueyuan ZhouClinic Services Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA. xueyuan.zhou@nih.gov.
Zhu LiuHainan Key Laboratory for Sustainable Utilization of Tropical Bioresources, College of Agriculture, Hainan University, Haikou, Hainan, 570228, China. zhuliu@hainu.edu.cn.
Jun ZhangDepartment of Chemistry, University of Alabama at Birmingham, Birmingham, AL, 35294, USA.
Joseph W AdelsbergerClinic Services Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA.
Jun YangClinic Services Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA.
Gregory F BurtonDepartment of Chemistry and Biochemistry, Brigham Young University, Provo, UT, 84602, USA.
Leidos (United States) · USBrigham Young University · USHainan University · CNUniversity of Alabama at Birmingham · US

Funding

Follicular dendritic cell activation and HIV pathogenesisR15AI091517 · NIAID · BRIGHAM YOUNG UNIVERSITY · PI BURTON, GREGORY F. · 2010 to 2010
$442k
NIAID NIH HHS R15 AI091517
6 · The paper itself

Abstract

backgroundStudy of a clinic case reveals that alpha-1-antitrypsin (AAT) deficiency is related to CD4+ T cell count decline and AIDS progression, suggesting that AAT might be an endogenous inhibitor of HIV/AIDS. Previous study shows that AAT inhibits HIV-1 replication in infected host cells and the C-terminus fragment of AAT, VIRIP, interferes with HIV-1 infection. However, it is still unclear whether and how intact AAT inhibits HIV-1 infection. It is also unknown what the mechanism of AAT is and which critical step(s) are involved.

resultsIn the present study, the C-terminus of AAT (C) was synthesized. C terminus-truncated AAT (ΔAAT) was also prepared by digesting AAT with metalloproteinase. Primary CD4+ T cells were then co-cultured with HIV-1 with the presence or absence of AAT/C/ΔAAT to detect cis-infection of HIV-1. The interaction between AAT/C/ΔAAT and gp120/gp41 was also measured. Meanwhile, HIV-1 reverse transcriptase activity and viral DNA integration were also detected in these lymphocytes. The results demonstrated that AAT and C, not ΔAAT, inhibited HIV-1 entry by directly interacting with gp41. Meanwhile, AAT, C and ΔAAT could not directly interfere with the steps of viral RNA reverse transcription and viral DNA integration.

conclusionAAT inhibits HIV-1 entry by directly interacting with gp41 through its C-terminus and thereby inhibits HIV-1 infection.

Indexed as

alpha 1-AntitrypsinCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesDNA, ViralHIV-1HIV Envelope Protein gp120HIV Envelope Protein gp41HIV InfectionsHIV Reverse TranscriptaseHumansIntegrasesMetalloproteasesProtein Interaction MapsReceptors, CCR5Receptors, CXCR4alpha 1-AntitrypsinCCR5 protein, humanCXCR4 protein, humanDNA, Viralgp41 protein, Human immunodeficiency virus 1HIV Envelope Protein gp120HIV Envelope Protein gp41HIV Reverse TranscriptaseIntegrasesMetalloproteasesReceptors, CCR5Receptors, CXCR4reverse transcriptase, Human immunodeficiency virus 1RNA, ViralAlpha-1-antitrypsingp41HIV-1IntegraseReverse transcriptase

Identifiers

PMID27473095
PMCPMC4966588
OpenAlexW2492230516

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.