Evidence map›Paper›PMID 38005838›Full record

ArticleViruses2023

Macrophage-Derived Factors with the Potential to Contribute to Pathogenicity of HIV-1 and HIV-2: Role of CCL-2/MCP-1.

Chunling Gao, Weiming Ouyang, Joseph Kutza, Tobias A Grimm, Karen Fields, Carla S R Lankford, Franziska Schwartzkopff, Mark Paciga, Tzanko Stantchev, Linda Tiffany and 2 more

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

Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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 2 institutions in 1 country.

Chunling GaoDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Weiming OuyangDivision of Biotechnology Review and Research 2, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Joseph KutzaDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Tobias A GrimmDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Karen FieldsDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Carla S R LankfordDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Franziska SchwartzkopffDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Mark PacigaDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Tzanko StantchevDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Linda TiffanyDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
Klaus StrebelLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.ORCID 0000-0002-2827-8923
Kathleen A ClouseDivision of Biotechnology Review and Research 1, Office of Biotechnology Products, Center for Drug Evaluation and Research, U. S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA.
United States Food and Drug Administration · USNational Institute of Allergy and Infectious Diseases · US

Funding

FDA HHS N/A
6 · The paper itself

Abstract

Human immunodeficiency virus type 2 (HIV-2) is known to be less pathogenic than HIV-1. However, the mechanism(s) underlying the decreased HIV-2 pathogenicity is not fully understood. Herein, we report that β-chemokine CCL2 expression was increased in HIV-1-infected human monocyte-derived macrophages (MDM) but decreased in HIV-2-infected MDM when compared to uninfected MDM. Inhibition of CCL2 expression following HIV-2 infection occurred at both protein and mRNA levels. By microarray analysis, quantitative PCR, and Western blotting, we identified that Signal Transducer and Activator of Transcription 1 (STAT1), a critical transcription factor for inducing CCL2 gene expression, was also reduced in HIV-2-infected MDM. Blockade of STAT1 in HIV-infected MDM using a STAT1 inhibitor significantly reduced the production of CCL2. In contrast, transduction of STAT1-expressing pseudo-retrovirus restored CCL2 production in HIV-2-infected MDM. These findings support the concept that CCL2 inhibition in HIV-2-infected MDM is meditated by reduction of STAT1. Furthermore, we showed that STAT1 reduction in HIV-2-infected MDM was regulated by the CUL2/RBX1 ubiquitin E3 ligase complex-dependent proteasome pathway. Knockdown of CUL2 or RBX1 restored the expression of STAT1 and CCL2 in HIV-2-infected MDM. Taken together, our findings suggest that differential regulation of the STAT1-CCL2 axis may be one of the mechanisms underlying the different pathogenicity observed for HIV-1 and HIV-2.

Indexed as

Chemokine CCL2HIV-1HIV-2HIV InfectionsCells, CulturedGene Expression RegulationHIV SeropositivityHumansMacrophagesVirulenceVirus ReplicationCCL2 protein, humanChemokine CCL2CCL2CULLIN 2HIV-1HIV-2macrophageRBX1STAT1

Identifiers

PMID38005838
PMCPMC10674259
OpenAlexW4387971986

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.