Evidence map›Paper›PMID 26317223›Full record

ArticlePloS one2015

Comparison of HIV-1 nef and gag Variations and Host HLA Characteristics as Determinants of Disease Progression among HIV-1 Vertically Infected Kenyan Children.

Matilda Chelimo Saina, Xiuqiong Bi, Raphael Lihana, Raphael Lwembe, Azumi Ishizaki, Annie Panikulam, Tresa Palakudy, Rachel Musoke, Mary Owens, Elijah Maritim Songok and 1 more

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Polymorphism rs1385129 Within Glut1 GeneFrontiers in immunology · 2018
    Article
  2. Article
  3. 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

11 authors at 3 institutions in 2 countries.

Matilda Chelimo SainaDepartment of Viral Infection and International Health, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Xiuqiong BiDepartment of Viral Infection and International Health, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Raphael LihanaCenter for Virus Research, Kenya Medical Research Institute, Nairobi, Kenya.
Raphael LwembeCenter for Virus Research, Kenya Medical Research Institute, Nairobi, Kenya.
Azumi IshizakiDepartment of Viral Infection and International Health, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Annie PanikulamNyumbani Children's home, Nairobi, Kenya.
Tresa PalakudyNyumbani Children's home, Nairobi, Kenya.
Rachel MusokeDepartment of pediatrics, University of Nairobi, Nairobi, Kenya.
Mary OwensNyumbani Children's home, Nairobi, Kenya.
Elijah Maritim SongokCenter for Virus Research, Kenya Medical Research Institute, Nairobi, Kenya.
Hiroshi IchimuraDepartment of Viral Infection and International Health, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Kanazawa University · JPKenya Medical Research Institute · KEUniversity of Nairobi · KE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDisease progression varies among HIV-1-infected individuals. The present study aimed to explore possible viral and host factors affecting disease progression in HIV-1-infected children.

methodsSince 2000, 102 HIV-1 vertically-infected children have been followed-up in Kenya. Here we studied 29 children (15 male/14 female) who started antiretroviral treatment at <5 years of age (rapid progressors; RP), and 32 (17 male/15 female) who started at >10 years of age (slow progressors; SP). Sequence variations in the HIV-1 gag and nef genes and the HLA class I-related epitopes were compared between the two groups.

resultsBased on nef sequences, HIV-1 subtypes A1/D were detected in 62.5%/12.5% of RP and 66.7%/20% of SP, with no significant difference in subtype distribution between groups (p = 0.8). In the ten Nef functional domains, only the PxxP3 region showed significantly greater variation in RP (33.3%) than SP (7.7%, p = 0.048). Gag sequences did not significantly differ between groups. The reportedly protective HLA-A alleles, A*74:01, A*32:01 and A*26, were more commonly observed in SP (50.0%) than RP (11.1%, p = 0.010), whereas the reportedly disease-susceptible HLA-B*45:01 was more common in RP (33.3%) than SP (7.4%, p = 0.045). Compared to RP, SP showed a significantly higher median number of predicted HLA-B-related 12-mer epitopes in Nef (3 vs. 2, p = 0.037), HLA-B-related 11-mer epitopes in Gag (2 vs. 1, p = 0.029), and HLA-A-related 9-mer epitopes in Gag (4 vs. 1, p = 0.051). SP also had fewer HLA-C-related epitopes in Nef (median 4 vs. 5, p = 0.046) and HLA-C-related 11-mer epitopes in Gag (median 1 vs. 1.5, p = 0.044) than RP.

conclusionsCompared to rapid progressors, slow progressors had more protective HLA-A alleles and more HLA-B-related epitopes in both the Nef and Gag proteins. These results suggest that the host factor HLA plays a stronger role in disease progression than the Nef and Gag sequence variations in HIV-1-infected Kenyan children.

Indexed as

Disease ProgressionGenetic VariationInfectious Disease Transmission, VerticalAdolescentAdultAllelesChildChild, PreschoolEpitopesFemalegag Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsHLA AntigensHost-Pathogen InteractionsHumansEpitopesgag Gene Products, Human Immunodeficiency VirusHLA Antigensnef Gene Products, Human Immunodeficiency Virus

Identifiers

PMID26317223
PMCPMC4552823
OpenAlexW1956443538

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.