Evidence map›Paper›PMID 21307185›Full record

ArticleJournal of virology2011

Epitope-specific CD8+ T lymphocytes cross-recognize mutant simian immunodeficiency virus (SIV) sequences but fail to contain very early evolution and eventual fixation of epitope escape mutations during SIV infection.

Evan M Cale, Peter Hraber, Elena E Giorgi, Will Fischer, Tanmoy Bhattacharya, Thomas Leitner, Wendy W Yeh, Cheryl Gleasner, Lance D Green, Cliff S Han and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  8. Clonality and intracellular polyploidy in virus evolution and pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2015
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  17. A quantitative quasispecies theory-based model of virus escape mutation under immune selection.Proceedings of the National Academy of Sciences of the United States of America · 2012
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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

12 authors at 4 institutions in 1 country.

Evan M CaleDivision of Viral Pathogenesis, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, E/CLS 1043, Boston, MA 02215, USA.
Peter Hraber
Elena E Giorgi
Will Fischer
Tanmoy Bhattacharya
Thomas Leitner
Wendy W Yeh
Cheryl Gleasner
Lance D Green
Cliff S Han
Bette Korber
Norman L Letvin
Los Alamos National Laboratory · USBeth Israel Deaconess Medical Center · USHarvard University · USJoint Genome Institute · US

Funding

Viral Sequencing CoreU19AI067854 · NIAID · DUKE UNIVERSITY · PI LETVIN, NORMAN L · 2006 to 2011
$290.5M
Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F · 2005 to 2005
$14.9M
NIAID NIH HHS AI067854NIAID NIH HHS U01 AI067854NIAID NIH HHS U19 AI067854
6 · The paper itself

Abstract

Human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) evade containment by CD8(+) T lymphocytes through focused epitope mutations. However, because of limitations in the numbers of viral sequences that can be sampled, traditional sequencing technologies have not provided a true representation of the plasticity of these viruses or the intensity of CD8(+) T lymphocyte-mediated selection pressure. Moreover, the strategy by which CD8(+) T lymphocytes contain evolving viral quasispecies has not been characterized fully. In the present study we have employed ultradeep 454 pyrosequencing of virus and simultaneous staining of CD8(+) T lymphocytes with multiple tetramers in the SIV/rhesus monkey model to explore the coevolution of virus and the cellular immune response during primary infection. We demonstrated that cytotoxic T lymphocyte (CTL)-mediated selection pressure on the infecting virus was manifested by epitope mutations as early as 21 days following infection. We also showed that CD8(+) T lymphocytes cross-recognized wild-type and mutant epitopes and that these cross-reactive cell populations were present at a time when mutant forms of virus were present at frequencies of as low as 1 in 22,000 sequenced clones. Surprisingly, these cross-reactive cells became enriched in the epitope-specific CD8(+) T lymphocyte population as viruses with mutant epitope sequences largely replaced those with epitope sequences of the transmitted virus. These studies demonstrate that mutant epitope-specific CD8(+) T lymphocytes that are present at a time when viral mutant epitope sequences are detected at extremely low frequencies fail to contain the later accumulation and fixation of the mutant epitope sequences in the viral quasispecies.

Indexed as

Evolution, MolecularMutation, MissenseAnimalsCD8-Positive T-LymphocytesCross ReactionsEpitopes, T-LymphocyteHigh-Throughput Nucleotide SequencingMacaca mulattaSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusT-Lymphocytes, CytotoxicEpitopes, T-Lymphocyte

Identifiers

PMID21307185
PMCPMC3126128
OpenAlexW2157908098

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.