Evidence map›Paper›PMID 23087435›Full record

ArticleThe Journal of infectious diseases2013

Reduced inflammation and lymphoid tissue immunopathology in rhesus macaques receiving anti-tumor necrosis factor treatment during primary simian immunodeficiency virus infection.

Brian Tabb, David R Morcock, Charles M Trubey, Octavio A Quiñones, Xing Pei Hao, Jeremy Smedley, Rhonda Macallister, Michael Piatak, Levelle D Harris, Mirko Paiardini and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 59 citations in OpenAlex.

  1. Lymph-Node-Based CD3Journal of virology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

Brian TabbAIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, SAIC-Frederick, Maryland, USA.
David R Morcock
Charles M Trubey
Octavio A Quiñones
Xing Pei Hao
Jeremy Smedley
Rhonda Macallister
Michael Piatak
Levelle D Harris
Mirko Paiardini
Guido Silvestri
Jason M Brenchley
W Gregory Alvord
Jeffrey D Lifson
Jacob D Estes
Emory University · USNational Institutes of Health · USScience Applications International Corporation (United States) · USData Management Services (United States) · 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
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

backgroundHuman immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections induce robust, generalized inflammatory responses that begin during acute infection and lead to pathological systemic immune activation, fibrotic damage of lymphoid tissues, and CD4⁺ T-cell loss, pathogenic processes that contribute to disease progression.

methodsTo better understand the contribution of tumor necrosis factor (TNF), a key regulator of acute inflammation, to lentiviral pathogenesis, rhesus macaques newly infected with SIVmac239 were treated for 12 weeks in a pilot study with adalimumab (Humira), a human anti-TNF monoclonal antibody.

resultsAdalimumab did not affect plasma SIV RNA levels or measures of T-cell immune activation (CD38 or Ki67) in peripheral blood or lymph node T cells. However, compared with untreated rhesus macaques, adalimumab-treated rhesus macaques showed attenuated expression of proinflammatory genes, decreased infiltration of polymorphonuclear cells into the T-cell zone of lymphoid tissues, and weaker antiinflammatory regulatory responses to SIV infection (ie, fewer presumed alternatively activated [ie, CD163⁺] macrophages, interleukin 10-producing cells, and transforming growth factor β-producing cells), along with reduced lymphoid tissue fibrosis and better preservation of CD4⁺ T cells.

conclusionsWhile HIV/SIV replication drives pathogenesis, these data emphasize the contribution of the inflammatory response to lentiviral infection to overall pathogenesis, and they suggest that early modulation of the inflammatory response may help attenuate disease progression.

Indexed as

Retroviruses, SimianAdalimumabAnimalsAntibodies, Monoclonal, HumanizedAnti-Inflammatory AgentsCD4 Lymphocyte CountCell MovementCytokinesFibrosisGene Expression RegulationInflammationLymph NodesLymphocyte ActivationMacaca mulattaMacrophagesMaleAdalimumabAntibodies, Monoclonal, HumanizedAnti-Inflammatory AgentsCytokinesRNA, ViralTumor Necrosis Factor-alpha

Identifiers

PMID23087435
PMCPMC3571439
OpenAlexW2121510700

What OpenQuestion holds

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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.