Evidence map›Paper›PMID 39502699›Full record

ArticleFrontiers in immunology2024

Acute-phase innate immune responses in SIVmac239-infected

Brandon C Rosen, Kaitlin Sawatzki, Michael J Ricciardi, Elise Smith, Inah Golez, Jack T Mauter, Núria Pedreño-López, Aaron Yrizarry-Medina, Kim L Weisgrau, Logan J Vosler and 13 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
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  4. Review
  5. 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

23 authors.

Brandon C RosenDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Kaitlin SawatzkiDepartment of Immunology, Center for Innate Immunity and Immune Disease, School of Medicine, University of Washington, Seattle, WA, United States.
Michael J RicciardiDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Elise SmithDepartment of Immunology, Center for Innate Immunity and Immune Disease, School of Medicine, University of Washington, Seattle, WA, United States.
Inah GolezDepartment of Immunology, Center for Innate Immunity and Immune Disease, School of Medicine, University of Washington, Seattle, WA, United States.
Jack T MauterDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Núria Pedreño-LópezDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Aaron Yrizarry-MedinaDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Kim L WeisgrauWisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, WI, United States.
Logan J VoslerWisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, WI, United States.
Thomas B VoigtDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Johan J LouwDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Jennifer Tisoncik-GoDepartment of Immunology, Center for Innate Immunity and Immune Disease, School of Medicine, University of Washington, Seattle, WA, United States.
Leanne S WhitmoreDepartment of Immunology, Center for Innate Immunity and Immune Disease, School of Medicine, University of Washington, Seattle, WA, United States.
Christakis PanayiotouDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Noor GhoshDepartment of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Jessica R FurlottWisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, WI, United States.
Christopher L ParksInternational AIDS Vaccine Initiative, New York, NY, United States.
Ronald C DesrosiersDepartment of Pathology, University of Miami Miller School of Medicine, Miami, FL, United States.
Jeffrey D LifsonAIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, MD, United States.
Eva G RakaszWisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, WI, United States.
David I Watkins *Department of Pathology, George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
Michael Gale *Department of Immunology, Center for Innate Immunity and Immune Disease, School of Medicine, University of Washington, Seattle, WA, United States.

Funding

Washington National Primate Research CenterP51OD010425 · OD · UNIVERSITY OF WASHINGTON · PI Mari Ostendorf · 2012 to 2026
$201.8M
WNPRC Supplemental Request for Nonhuman Primate Enclosures to Equip HIV/AIDS-Related Research FacilitiesP51OD011106 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI Dorota A. Grejner-Brzezinska · 2012 to 2026
$150.7M
NIH HHS P51 OD010425NIH HHS P51 OD011106
6 · The paper itself

Abstract

Introduction: Spontaneous control of chronic-phase HIV/SIV viremia is often associated with the expression of specific MHC class I allotypes. HIV/SIV-specific CD8+ cytotoxic T lymphocytes (CTLs) restricted by these MHC class I allotypes appear to be critical for viremic control. Establishment of the elite controller (EC) phenotype is predictable in SIVmac239-infected Indian rhesus macaques (RMs), with approximately 50% of Methods: To gain insight into the immunological factors involved in the determination of EC status, we vaccinated 16 Results: Vaccination did not provide protection against acquisition, but peak and setpoint viremia were significantly lower in vaccinees relative to controls. We did not identify any meaningful correlations between vaccine-induced CTL parameters and SIVmac239 acquisition rate or chronic-phase viral loads. Ultimately, 13 of 16 vaccinees (81%) and 7 of 16 controls (44%) became ECs (viremia ≤ 10,000 vRNA copies/mL plasma for ≥ 4 weeks). We identified subsets of immunomodulatory genes differentially expressed (DE) between RM groupings based on vaccination status, EC status, and MHC class I genotype. These DE genes function in multiple innate immune processes, including the complement system, cytokine/chemokine signaling, pattern recognition receptors, and interferon-mediated responses. Discussion: A striking difference in the kinetics of differential gene expression among our RM groups suggests that

Indexed as

Immunity, InnateMacaca mulattaSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusViral LoadViremiaAnimalsHistocompatibility Antigens Class IT-Lymphocytes, CytotoxicHistocompatibility Antigens Class Iacquired immunodeficiency syndrome (AIDS)cytotoxic T lymphocytes (CTLs)human immunodeficiency virus (HIV)simian immunodeficiency virus (SIV)vaccines

Identifiers

PMID39502699
PMCPMC11534762

What OpenQuestion holds

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Registered trials

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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.