Evidence map›Paper›PMID 24667791›Full record

Trial reportPloS one2014

Lack of association between intact/deletion polymorphisms of the APOBEC3B gene and HIV-1 risk.

Mayumi Imahashi, Taisuke Izumi, Dai Watanabe, Junji Imamura, Kazuhiro Matsuoka, Hirotaka Ode, Takashi Masaoka, Kei Sato, Noriyo Kaneko, Seiichi Ichikawa and 8 more

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. The current toolbox for APOBEC drug discovery.Trends in pharmacological sciences · 2022
    Review
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  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. The 30 kb deletion in theOncotarget · 2017
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

18 authors at 6 institutions in 1 country.

Mayumi ImahashiDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan; Department of Hematology and Oncology, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Taisuke IzumiDepartment of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Japanese Foundation for AIDS Prevention, Chiyoda-ku, Tokyo, Japan.
Dai WatanabeClinical Research Center, National Hospital Organization Osaka Medical Center, Osaka Japan.
Junji ImamuraDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Kazuhiro MatsuokaDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Hirotaka OdeDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Takashi MasaokaDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Kei SatoCenter for Human Retrovirus Research, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Noriyo KanekoDepartment of International Health Nursing, Graduate School of Nursing, Nagoya City University, Nagoya, Japan.
Seiichi IchikawaDepartment of International Health Nursing, Graduate School of Nursing, Nagoya City University, Nagoya, Japan.
Yoshio KoyanagiCenter for Human Retrovirus Research, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Akifumi Takaori-KondoDepartment of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Makoto UtsumiDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Yoshiyuki YokomakuDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Takuma ShirasakaClinical Research Center, National Hospital Organization Osaka Medical Center, Osaka Japan.
Wataru SugiuraDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan; Department of AIDS Research, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Yasumasa IwataniDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan; Department of AIDS Research, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Tomoki NaoeDepartment of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan; Department of Hematology and Oncology, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Kyoto University · JPNational Hospital Organization · JPNagoya Medical Center · JPNagoya University · JPNagoya City University · JPOsaka National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe human APOBEC3 family of proteins potently restricts HIV-1 replication APOBEC3B, one of the family genes, is frequently deleted in human populations. Two previous studies reached inconsistent conclusions regarding the effects of APOBEC3B loss on HIV-1 acquisition and pathogenesis. Therefore, it was necessary to verify the effects of APOBEC3B on HIV-1 infection in vivo.

methodsIntact (I) and deletion (D) polymorphisms of APOBEC3B were analyzed using PCR. The syphilis, HBV and HCV infection rates, as well as CD4(+) T cell counts and viral loads were compared among three APOBEC3B genotype groups (I/I, D/I, and D/D). HIV-1 replication kinetics was assayed in vitro using primary cells derived from PBMCs.

resultsA total of 248 HIV-1-infected Japanese men who have sex with men (MSM) patients and 207 uninfected Japanese MSM were enrolled in this study. The genotype analysis revealed no significant differences between the APOBEC3B genotype ratios of the infected and the uninfected cohorts (p = 0.66). In addition, HIV-1 disease progression parameters were not associated with the APOBEC3B genotype. Furthermore, the PBMCs from D/D and I/I subjects exhibited comparable HIV-1 susceptibility.

conclusionOur analysis of a population-based matched cohort suggests that the antiviral mechanism of APOBEC3B plays only a negligible role in eliminating HIV-1 in vivo.

Indexed as

Genetic Predisposition to DiseaseHIV-1Polymorphism, GeneticAdultAsian PeopleCohort StudiesCytidine DeaminaseHIV InfectionsHumansJapanMaleMiddle AgedMinor Histocompatibility AntigensAPOBEC3B protein, humanCytidine DeaminaseMinor Histocompatibility Antigens

Identifiers

PMID24667791
PMCPMC3965477
OpenAlexW2018507313

What OpenQuestion holds

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LicenceCC BY
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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.