Evidence map›Paper›PMID 32426577›Full record

ArticlePathogens & immunity2020

Biomarkers of Cellular Stress Do Not Associate with sCD14 in Progressive HIV and SIV Infections

Carol L Vinton, Carly E Starke, Alexandra M Ortiz, Stephen H Lai, Jacob K Flynn, Ornella Sortino, Kenneth Knox, Irini Sereti, Jason M Brenchley

Open access · diamondAbstract read
In one paragraph

Article in Pathogens & immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Carol L VintonBarrier Immunity Section; Laboratory of Viral Diseases; NIAID, NIH; Bethesda, Maryland.
Carly E StarkeBarrier Immunity Section; Laboratory of Viral Diseases; NIAID, NIH; Bethesda, Maryland.
Alexandra M OrtizBarrier Immunity Section; Laboratory of Viral Diseases; NIAID, NIH; Bethesda, Maryland.
Stephen H LaiBarrier Immunity Section; Laboratory of Viral Diseases; NIAID, NIH; Bethesda, Maryland.
Jacob K FlynnBarrier Immunity Section; Laboratory of Viral Diseases; NIAID, NIH; Bethesda, Maryland.
Ornella SortinoHIV Pathogenesis Section; Laboratory of Immunoregulation; NIAID, NIH; Bethesda, Maryland.
Kenneth KnoxDepartment of Medicine; University of Arizona; Tucson, Arizona.
Irini SeretiHIV Pathogenesis Section; Laboratory of Immunoregulation; NIAID, NIH; Bethesda, Maryland.
Jason M BrenchleyBarrier Immunity Section; Laboratory of Viral Diseases; NIAID, NIH; Bethesda, Maryland.
National Institutes of Health · USOffice of Extramural Research · USGlobal Viral · USUniversity of Arizona · US

Funding

Mechanisms of Immune Activation and Disease Progression in Animal ModelsZIAAI001029 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BRENCHLEY, JASON · 2009 to 2025
$28.2M
6 · The paper itself

Abstract

backgroundMicrobial translocation occurs after damage to the structural and/or immunological barrier of the gastrointestinal (GI) tract into circulation. Microbial components that trans-locate from the lumen of the GI tract directly stimulate the immune system and contribute to inflammation. When microbial translocation becomes chronic, the inflammation has detrimental consequences. Given that microbial translocation is an important phenomenon in many diseases, defining biomarkers that reliably reflect microbial translocation is critical. Measurement of systemic microbial products is difficult since: 1) robust assays to measure microbial antigens simultaneously are lacking; 2) confounding factors influence assays used to detect microbial products; and 3) biological clearance mechanisms limit their detection in circulation. Thus, host proteins produced in response to microbial stimulation are used as surrogates for microbial translocation; however, many of these proteins are also produced in response to host proteins expressed by dying cells.

methodsWe measured plasma levels of biomarkers associated with GI tract damage, immune responses to microbial products, and cell-death in people living with HIV before and after antiretroviral administration, and in macaque nonhuman primates before and after SIV infection.

resultsProteins secreted during cellular stress (receptor for advanced glycation endproducts-RAGE and high motility group box 1-HMGB1), which can induce sCD14 production

conclusionsBystander cell death and generalized inflammation do not contribute to elevated levels of sCD14 observed in HIV/SIV-infected individuals.

Indexed as

HIVinflammationMicrobial translocationSIV

Identifiers

PMID32426577
PMCPMC7224679
OpenAlexW3023200688

What OpenQuestion holds

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LicenceCC BY
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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.