Evidence map›Paper›PMID 10852125›Full record

ReviewImmunologic research2000

Virus and target cell evolution in human immunodeficiency virus type 1 infection.

D E Mosier

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Trade-offs in antibody repertoires to complex antigens.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Article
  4. Review
  5. Progress on RNAi-based molecular medicines.International journal of nanomedicine · 2012
    Review
  6. Good cell, bad cell: flow cytometry reveals T-cell subsets important in HIV disease.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2010
    Review
  7. Article
  8. Article
  9. Article
  10. 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

1 author at 1 institution in 1 country.

D E MosierDepartment of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA. dmosier@scripps.edu
Scripps Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus (HIV) infection leads to a prolonged struggle between a rapidly evolving viral population and a potent immune response. In the vast majority of infected individuals, the virus wins this struggle. In my laboratory, we focus on understanding both the viral and immune factors that contribute to this outcome. The results of our studies and those of many others indicate that HIV can escape a potent immune response by a combination of mechanisms including rapid mutation, shedding of decoy antigens, modulation of host major histocompatibility complex, and destruction of cytotoxic T lymphocytes. The target cells for viral infection change as the virus evolves to use different chemokine coreceptors for entry. The initial targets are activated and resting memory T cells that express both CD4 and CCR5, but both naive and memory CD4 T cells are targeted by viruses capable of using CXCR4 for entry, and macrophages become the primary target cells when most CD4 T cells are depleted. Compelling evidence is emerging that the availability of target cells for infection is as limiting for the spread of virus as the immune response.

Indexed as

HIV-1HIV InfectionsHumansImmunity, CellularT-Lymphocyte Subsets

Identifiers

PMID10852125
OpenAlexW2028774908

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.