Evidence map›Paper›PMID 21625590›Full record

ArticlePLoS pathogens2011

Viral CTL escape mutants are generated in lymph nodes and subsequently become fixed in plasma and rectal mucosa during acute SIV infection of macaques.

Thomas H Vanderford, Chelsea Bleckwehl, Jessica C Engram, Richard M Dunham, Nichole R Klatt, Mark B Feinberg, David A Garber, Michael R Betts, Guido Silvestri

Abstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Article
  2. Article
  3. CD8Nature microbiology · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Genetically barcoded SIV reveals the emergence of escape mutations in multiple viral lineages during immune escape.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Mechanisms of CD8European journal of immunology · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors.

Thomas H VanderfordYerkes National Primate Research Center, Emory University, Atlanta, Georgia, United States of America.
Chelsea Bleckwehl
Jessica C Engram
Richard M Dunham
Nichole R Klatt
Mark B Feinberg
David A Garber
Michael R Betts
Guido Silvestri

Funding

Project Coordination and Product DevelopmentU19AI061728 · NIAID · EMORY UNIVERSITY · PI ALTMAN, JOHN D · 2004 to 2008
$14.3M
TRAINING IN HIV PATHOGENESIST32AI007632 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI Frederic D Bushman, James L. Riley · 2000 to 2026
$10.6M
NIAID NIH HHS T32 AI007632NIAID NIH HHS T32AI007632-10NIAID NIH HHS U19 AI061728NIAID NIH HHS U19-AI061728
6 · The paper itself

Abstract

SIV(mac239) infection of rhesus macaques (RMs) results in AIDS despite the generation of a strong antiviral cytotoxic T lymphocyte (CTL) response, possibly due to the emergence of viral escape mutants that prevent recognition of infected cells by CTLs. To determine the anatomic origin of these SIV mutants, we longitudinally assessed the presence of CTL escape variants in two MamuA*01-restricted immunodominant epitopes (Tat-SL8 and Gag-CM9) in the plasma, PBMCs, lymph nodes (LN), and rectal biopsies (RB) of fifteen SIV(mac239)-infected RMs. As expected, Gag-CM9 did not exhibit signs of escape before day 84 post infection. In contrast, Tat-SL8 escape mutants were apparent in all tissues by day 14 post infection. Interestingly LNs and plasma exhibited the highest level of escape at day 14 and day 28 post infection, respectively, with the rate of escape in the RB remaining lower throughout the acute infection. The possibility that CTL escape occurs in LNs before RBs is confirmed by the observation that the specific mutants found at high frequency in LNs at day 14 post infection became dominant at day 28 post infection in plasma, PBMC, and RB. Finally, the frequency of escape mutants in plasma at day 28 post infection correlated strongly with the level Tat-SL8-specific CD8 T cells in the LN and PBMC at day 14 post infection. These results indicate that LNs represent the primary source of CTL escape mutants during the acute phase of SIV(mac239) infection, suggesting that LNs are the main anatomic sites of virus replication and/or the tissues in which CTL pressure is most effective in selecting SIV escape variants.

Indexed as

AnimalsGenes, gagGenes, tatImmunodominant EpitopesIntestinal MucosaLymph NodesMacaca mulattaMolecular Sequence DataRectumSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusT-Lymphocytes, CytotoxicVirus ReplicationImmunodominant Epitopes

Identifiers

PMID21625590
PMCPMC3098234

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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.