Evidence map›Paper›PMID 34765923›Full record

ArticleiScience2021

Prestimulation of CD2 confers resistance to HIV-1 latent infection in blood resting CD4 T cells.

Sijia He, Jia Guo, Yajing Fu, Mark Spear, Chaolong Qin, Shuai Fu, Zongqiang Cui, Wenwen Jin, Xuehua Xu, Wanjun Chen and 2 more

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

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

12 authors at 4 institutions in 2 countries.

Sijia HeNHC Key Laboratory of AIDS Immunology (China Medical University), National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Jia GuoCenter for Infectious Disease Research, School of Systems Biology, George Mason University, Manassas, VA 20110, USA.
Yajing FuNHC Key Laboratory of AIDS Immunology (China Medical University), National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Mark SpearCenter for Infectious Disease Research, School of Systems Biology, George Mason University, Manassas, VA 20110, USA.
Chaolong QinNHC Key Laboratory of AIDS Immunology (China Medical University), National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Shuai FuNHC Key Laboratory of AIDS Immunology (China Medical University), National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Zongqiang CuiCenter for Infectious Disease Research, School of Systems Biology, George Mason University, Manassas, VA 20110, USA.
Wenwen JinMucosal Immunology Section, NIDCR, NIH, Bethesda, MD 20892, USA.
Xuehua XuChemotaxis Signal Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Disease, NIH, Twinbrook Facility, Rockville, MD 20852, USA.
Wanjun ChenMucosal Immunology Section, NIDCR, NIH, Bethesda, MD 20892, USA.
Hong ShangNHC Key Laboratory of AIDS Immunology (China Medical University), National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Yuntao WuCenter for Infectious Disease Research, School of Systems Biology, George Mason University, Manassas, VA 20110, USA.
George Mason University · USChina Medical University · CNNational Institute of Dental and Craniofacial Research · USNational Institute of Allergy and Infectious Diseases · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV-1 infects blood CD4 T cells through the use of CD4 and CXCR4 or CCR5 receptors, which can be targeted through blocking viral binding to CD4/CXCR4/CCR5 or virus-cell fusion. Here we describe a novel mechanism by which HIV-1 nuclear entry can also be blocked through targeting a non-entry receptor, CD2. Cluster of differentiation 2 (CD2) is an adhesion molecule highly expressed on human blood CD4, particularly, memory CD4 T cells. We found that CD2 ligation with its cell-free ligand LFA-3 or anti-CD2 antibodies rendered blood resting CD4 T cells highly resistant to HIV-1 infection. We further demonstrate that mechanistically, CD2 binding initiates competitive signaling leading to cofilin activation and localized actin polymerization around CD2, which spatially inhibits HIV-1-initiated local actin polymerization needed for viral nuclear migration. Our study identifies CD2 as a novel target to block HIV-1 infection of blood resting T cells.

Indexed as

Immune responseImmunologyVirology

Identifiers

PMID34765923
PMCPMC8571718
OpenAlexW3207262412

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.