Evidence map›Paper›PMID 17267483›Full record

ArticleJournal of virology2007

Susceptibility of CCR5-deficient mice to genital herpes simplex virus type 2 is linked to NK cell mobilization.

Manoj Thapa, William A Kuziel, Daniel J J Carr

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 112 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. IFN-bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Natural killer cells in antiviral immunity.Nature reviews. Immunology · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

11 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Manoj ThapaDepartment of Microbiology, DMEI #415, The University of Oklahoma Health Sciences Center, 608 Stanton L. Young Blvd., Oklahoma City, OK 73104, USA.
William A Kuziel
Daniel J J Carr
Ophthalmology Associates (United States) · USPDL BioPharma (United States) · US

Funding

The Neuroimmunology of Viral InfectionR01AI053108 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CARR, DANIEL J · 2003 to 2022
$5.8M
CORE--MOLECULAR BIOLOGYP30EY012190 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ANDERSON, ROBERT E · 1999 to 2009
$5.2M
NEI NIH HHS EY12190NEI NIH HHS P30 EY012190NIAID NIH HHS AI053108NIAID NIH HHS R01 AI053108
6 · The paper itself

Abstract

Following genital herpes simplex virus type 2 (HSV-2) exposure, NK cells and T cells are mobilized to sites of infection to control viral replication and spread. The present investigation sought to determine the role of the chemokine receptor CCR5 in this process. Mice deficient in CCR5 (CCR5-/-) displayed a significant reduction in cumulative survival following infection in comparison to wild-type, HSV-2-infected controls. Associated with decreased resistance to viral infection, CCR5-/- mice yielded significantly more virus and expressed higher levels of tumor necrosis factor alpha, CXCL1, CCL2, CCL3, and CCL5 in the vagina, spinal cord, and/or brain stem than did wild-type mice. Whereas there was no difference in absolute number of leukocytes (CD45high), CD4 T cells, or CD8 T cells residing in the draining lymph nodes, spleen, spinal cord, or brain stem comparing HSV-2-infected wild-type to CCR5-/- mice prior to or after infection, there were significantly more NK cells (NK1.1+ CD3-) residing in the brain stem and spleen of infected wild-type mice. Functionally, NK activity from cells isolated from the brain stem of HSV-2-infected wild-type mice was greater than that from HSV-2-infected CCR5-/- mice. In addition, antibody-mediated depletion of NK cells resulted in an increase in HSV-2 levels in the vaginal, spinal cord, and brain stem tissue of wild-type but not CCR5-/- mice. Collectively, the absence of CCR5 expression significantly impacts the ability of the host to control genital HSV-2 infection, inflammation, and spread associated with a specific reduction in NK cell expansion, infiltration, and activity in the nervous system.

Indexed as

Immunity, InnateAnimalsBrain StemChemokinesDisease Models, AnimalFemaleGene ExpressionGranzymesHerpes GenitalisHerpesvirus 2, HumanKiller Cells, NaturalLeukocyte Reduction ProceduresMiceMice, Inbred C57BLMice, KnockoutPore Forming Cytotoxic ProteinsChemokinesGranzymesperforin, mousePore Forming Cytotoxic ProteinsReceptors, CCR5

Identifiers

PMID17267483
PMCPMC1866094
OpenAlexW2170739757

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.