Evidence map›Paper›PMID 27322772›Full record

ArticleThe American journal of pathology2016

Splenic Damage during SIV Infection: Role of T-Cell Depletion and Macrophage Polarization and Infection.

Dionna W Williams, Elizabeth L Engle, Erin N Shirk, Suzanne E Queen, Lucio Gama, Joseph L Mankowski, M Christine Zink, Janice E Clements

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. IBA-1Research square · 2026
    Article
  3. Article
  4. Article
  5. IL-27 effects on HIVFrontiers in virology (Lausanne, Switzerland) · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Marked Enteropathy in an Accelerated Macaque Model of AIDS.The American journal of pathology · 2017
    Article
  19. Article
  20. Review
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

8 authors at 2 institutions in 1 country.

Dionna W WilliamsDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Elizabeth L EngleDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Erin N ShirkDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Suzanne E QueenDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Lucio GamaDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Joseph L MankowskiDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
M Christine ZinkDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Janice E ClementsDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Electronic address: jclements@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Project 4: Intracellular mechanism of virus persistence in astrocytes/macrophagesP01MH070306 · NIMH · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2004 to 2015
$16.0M
Viral Testing CoreU42OD013117 · OD · JOHNS HOPKINS UNIVERSITY · PI Lydia Hopper · 2017 to 2026
$10.9M
Development of an SPF Macaca nemestrina Breeding ColonyP40OD013117 · OD · JOHNS HOPKINS UNIVERSITY · PI ADAMS, ROBERT J. · 2012 to 2016
$4.9M
Novel SIV Model of HANDR01NS077869 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E, MANKOWSKI, JOSEPH L · 2012 to 2016
$3.8M
Plasma miRNA Biomarkers of HIV/SIV CNS DiseaseR01NS076357 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2012 to 2016
$2.7M
Macrophage Polarization in SIV Infection and LatencyR56AI118753 · NIAID · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2015 to 2015
$773k
NIAID NIH HHS R56 AI118753NIH HHS P40 OD013117NIH HHS U42 OD013117NIMH NIH HHS P01 MH070306NINDS NIH HHS R01 NS076357NINDS NIH HHS R01 NS077869
6 · The paper itself

Abstract

The effects of HIV infection on spleen and its cellular subsets have not been fully characterized, particularly for macrophages in which diverse populations exist. We used an accelerated SIV-infected macaque model to examine longitudinal effects on T-cell and macrophage populations and their susceptibilities to infection. Substantial lymphoid depletion occurred, characterized by follicular burn out and a loss of CD3 T lymphocytes, which was associated with cellular activation and transient dysregulations in CD4/CD8 ratios and memory effector populations. In contrast, the loss of CD68 and CD163(+)CD68(+) macrophages and increase in CD163 cells was irreversible, which began during acute infection and persisted until terminal disease. Mac387 macrophages and monocytes were transiently recruited into spleen, but were not sufficient to mitigate the changes in macrophage subsets. Type I interferon, M2 polarizing genes, and chemokine-chemokine receptor signaling were up-regulated in spleen and drove macrophage alterations. SIV-infected T cells were numerous within the white pulp during acute infection, but were rarely observed thereafter. CD68, CD163, and Mac387 macrophages were highly infected, which primarily occurred in the red pulp independent of T cells. Few macrophages underwent apoptosis, indicating that they are a long-lasting target for HIV/SIV. Our results identify macrophages as an important contributor to HIV/SIV infection in spleen and in promoting morphologic changes through the loss of specific macrophage subsets that mediate splenic organization.

Indexed as

AnimalsImmunohistochemistryIn Situ HybridizationMacaca nemestrinaMacrophagesOligonucleotide Array Sequence AnalysisSimian Acquired Immunodeficiency SyndromeSpleenT-Lymphocytes

Identifiers

PMID27322772
PMCPMC4973662
OpenAlexW2441128872

What OpenQuestion holds

Textmetadata
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.