Evidence map›Paper›PMID 11519478›Full record

ArticleJournal of neurovirology2001

Functional analyses of natural killer cells in macaques infected with neurovirulent simian immunodeficiency virus.

T M Shieh, D L Carter, R L Blosser, J L Mankowski, M C Zink, J E Clements

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Journal of neurovirology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.5field-weighted citation impact, top 43% 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, 32 citations in OpenAlex.

  1. Trial
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  5. Observational
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  12. Ischemic neurons recruit natural killer cells that accelerate brain infarction.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. IL-23 in infections, inflammation, autoimmunity and cancer: possible role in HIV-1 and AIDS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012
    Review
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

T M ShiehDivision of Comparative Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
D L Carter
R L Blosser
J L Mankowski
M C Zink
J E Clements
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

CD4 INDEPENDENT ENTRY OF SIV IN THE CNSR01NS038008 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE ELLEN · 1998 to 2002
$1.1M
MOLECULAR PATHOGENESIS OF AIDS RELATED CNS DISEASET32NS007392 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE ELLEN · 1995 to 2005
$895k
VIRUS AND HOST FACTORS IN SIV ENCEPHALITISR01NS036911 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ZINK, M CHRISTINE · 1997 to 2000
$299k
NEUROFILAMENT PROTEINS--ASSEMBLY AND AXONAL TRANSPORTR15NS035344 · NINDS · OHIO UNIVERSITY ATHENS · PI BROWN, ANTHONY · 1996 to 1996
–
NHLBI NIH HHS HL03833NINDS NIH HHS NS07392NINDS NIH HHS NS35344NINDS NIH HHS NS36911NINDS NIH HHS NS38008
6 · The paper itself

Abstract

Clearance of HIV and SIV from the peripheral blood by the cellular immune system lessens the viral burden in infected individuals and may have an impact on virus infection of the CNS and the development of CNS lesions. However, the role of immune responses in preventing or limiting CNS infection has not been clearly defined. We investigated the role of natural killer cells in the outcome of SIV infection of macaques as a model for humans with AIDS and HIV encephalitis. In our study, six pig-tailed macaques were infected with the neurovirulent virus, SIV/17E-Fr, and the immunosuppressive virus, SIV/ DeltaB670, in a model system that causes rapid progression to AIDS and a high frequency of CNS lesions. NK lytic activity in each macaque was monitored longitudinally. In addition, we enumerated NK cells and tested macaque PBMC for the ability to lyse SIV-infected target cells. We found that there was a significant inverse correlation (P=0.02) between the robustness of NK response and the development of CNS lesions. Animals lacking strong NK cell responses developed more severe CNS lesions than those with robust NK responses did. Furthermore, pre-infection levels of NK activity were predictive of CNS lesion severity. The macaque with the most robust pre-infection NK activity developed no CNS lesions. In these infected macaques, NK activity was shown to be directed against SIV-infected cells. We extended these in vivo findings to delineate precisely which cell type was mediating this SIV-directed lysis. We used both macaque and human cells to demonstrate that the population that mediated anti-SIV and anti-HIV cytolytic effects was NK cells. Furthermore, we showed that this anti-SIV and anti-HIV cytolytic effect was directed at the envelope protein and not gag proteins. Thus, NK cells have the capacity to recognize and lyse cells expressing SIV and HIV antigens. These data support a role for NK cells in the modulation of CNS disease.

Indexed as

Acute DiseaseAIDS Dementia ComplexAnimalsBrainCD4 Lymphocyte CountCD4-Positive T-LymphocytesCD56 AntigenCell CountCells, CulturedCytotoxicity, ImmunologicCytotoxicity Tests, ImmunologicDisease Models, AnimalDisease ProgressionHIV-1HumansKiller Cells, NaturalCD56 AntigenViral Envelope Proteins

Identifiers

PMID11519478
OpenAlexW2119357333

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.