Evidence map›Paper›PMID 32479976›Full record

ReviewVirus research2020

Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.

Joel Henrique Ellwanger, Bruna Kulmann-Leal, Valéria de Lima Kaminski, Andressa Gonçalves Rodrigues, Marcelo Alves de Souza Bragatte, José Artur Bogo Chies

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Virus research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.2field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Effect ofMicroorganisms · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Legacy of a magic gene-Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Joel Henrique EllwangerLaboratório de Imunobiologia e Imunogenética, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil; Programa de Pós-Graduação em Genética e Biologia Molecular, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil.
Bruna Kulmann-LealLaboratório de Imunobiologia e Imunogenética, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil; Programa de Pós-Graduação em Genética e Biologia Molecular, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil.
Valéria de Lima KaminskiLaboratório de Imunobiologia e Imunogenética, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil; Programa de Pós-Graduação em Genética e Biologia Molecular, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil; Programa de Pós-Graduação em Biotecnologia, Laboratório de Imunologia Aplicada, Instituto de Ciência e Tecnologia - ICT, Universidade Federal de São Paulo - UNIFESP, São José dos Campos, São Paulo, Brazil.
Andressa Gonçalves RodriguesLaboratório de Imunobiologia e Imunogenética, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil.
Marcelo Alves de Souza BragattePrograma de Pós-Graduação em Genética e Biologia Molecular, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil; Núcleo de Bioinformática do Laboratório de Imunobiologia e Imunogenética, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil.
José Artur Bogo ChiesLaboratório de Imunobiologia e Imunogenética, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil; Programa de Pós-Graduação em Genética e Biologia Molecular, Departamento de Genética, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Brazil. Electronic address: jabchies@terra.com.br.
Universidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interactions between chemokine receptors and their ligands may affect susceptibility to infectious diseases as well as their clinical manifestations. These interactions mediate both the traffic of inflammatory cells and virus-associated immune responses. In the context of viral infections, the human C-C chemokine receptor type 5 (CCR5) receives great attention from the scientific community due to its role as an HIV-1 co-receptor. The genetic variant CCR5Δ32 (32 base-pair deletion in CCR5 gene) impairs CCR5 expression on the cell surface and is associated with protection against HIV infection in homozygous individuals. Also, the genetic variant CCR5Δ32 modifies the CCR5-mediated inflammatory responses in various conditions, such as inflammatory and infectious diseases. CCR5 antagonists mimic, at least in part, the natural effects of the CCR5Δ32 in humans, which explains the growing interest in the potential benefits of using CCR5 modulators for the treatment of different diseases. Nevertheless, beyond HIV infection, understanding the effects of the CCR5Δ32 variant in multiple viral infections is essential to shed light on the potential effects of the CCR5 modulators from a broader perspective. In this context, this review discusses the involvement of CCR5 and the effects of the CCR5Δ32 in human infections caused by the following pathogens: West Nile virus, Influenza virus, Human papillomavirus, Hepatitis B virus, Hepatitis C virus, Poliovirus, Dengue virus, Human cytomegalovirus, Crimean-Congo hemorrhagic fever virus, Enterovirus, Japanese encephalitis virus, and Hantavirus. Subsequently, this review addresses the impacts of CCR5 gene editing and CCR5 modulation on health and viral diseases. Also, this article connects recent findings regarding extracellular vesicles (e.g., exosomes), viruses, and CCR5. Neglected and emerging topics in "CCR5 research" are briefly described, with focus on Rocio virus, Zika virus, Epstein-Barr virus, and Rhinovirus. Finally, the potential influence of CCR5 on the immune responses to coronaviruses is discussed.

Indexed as

AnimalsFlavivirusGenetic VariationGenotypeHIV-1HIV InfectionsHumansMiceReceptors, CCR5Virus DiseasesCCR5 protein, humanReceptors, CCR5C-C chemokine receptor type 5ChemokineHost-pathogen interactionsImmunogeneticsInflammationViral infection

Identifiers

PMID32479976
PMCPMC7260533
OpenAlexW3029292308

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.