Evidence map›Paper›PMID 25406087›Full record

ArticlePloS one2014

Host genetic factors associated with symptomatic primary HIV infection and disease progression among Argentinean seroconverters.

Romina Soledad Coloccini, Dario Dilernia, Yanina Ghiglione, Gabriela Turk, Natalia Laufer, Andrea Rubio, María Eugenia Socías, María Inés Figueroa, Omar Sued, Pedro Cahn and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. A SYSTEMATIC REVIEW ON THE INFLUENCE OF HLA-B POLYMORPHISMS ON HIV-1 MOTHER-TO-CHILD-TRANSMISSION.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. 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

13 authors at 6 institutions in 1 country.

Romina Soledad ColocciniInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
Dario DilerniaInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
Yanina GhiglioneInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
Gabriela TurkInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
Natalia LauferInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina; Hospital Juan A. Fernandez, Buenos Aires, Argentina.
Andrea RubioInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
María Eugenia SocíasHospital Juan A. Fernandez, Buenos Aires, Argentina; Fundación Huésped, Buenos Aires, Argentina.
María Inés FigueroaHospital Juan A. Fernandez, Buenos Aires, Argentina; Fundación Huésped, Buenos Aires, Argentina.
Omar SuedHospital Juan A. Fernandez, Buenos Aires, Argentina; Fundación Huésped, Buenos Aires, Argentina.
Pedro CahnHospital Juan A. Fernandez, Buenos Aires, Argentina; Fundación Huésped, Buenos Aires, Argentina.
Horacio SalomónInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
Andrea ManganoLaboratorio de Biología Celular y Retrovirus, CONICET, Hospital de Pediatría "Prof. Dr. Juan P. Garrahan", Buenos Aires, Argentina.
María Ángeles PandoInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.
Fundación Huésped · ARInstituto de Investigaciones Biomédicas en Retrovirus y Sida · ARUniversity of Buenos Aires · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARGarrahan Hospital · ARHospital Fernández · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVariants in HIV-coreceptor C-C chemokine receptor type 5 (CCR5) and Human leukocyte antigen (HLA) genes are the most important host genetic factors associated with HIV infection and disease progression. Our aim was to analyze the association of these genetic factors in the presence of clinical symptoms during Primary HIV Infection (PHI) and disease progression within the first year.

methodsSeventy subjects diagnosed during PHI were studied (55 symptomatic and 15 asymptomatic). Viral load (VL) and CD4 T-cell count were evaluated. HIV progression was defined by presence of B or C events and/or CD4 T-cell counts <350 cell/mm3. CCR5 haplotypes were characterized by polymerase chain reaction and SDM-PCR-RFLP. HLA-I characterization was performed by Sequencing.

resultsSymptoms during PHI were significantly associated with lower frequency of CCR5-CF1 (1.8% vs. 26.7%, p = 0.006). Rapid progression was significantly associated with higher frequency of CCR5-CF2 (16.7% vs. 0%, p = 0.024) and HLA-A*11 (16.7% vs. 1.2%, p = 0.003) and lower frequency of HLA-C*3 (2.8% vs. 17.5%, p = 0.035). Higher baseline VL was significantly associated with presence of HLA-A*11, HLA-A*24, and absence of HLA-A*31 and HLA-B*57. Higher 6-month VL was significantly associated with presence of CCR5-HHE, HLA-A*24, HLA-B*53, and absence of HLA-A*31 and CCR5-CF1. Lower baseline CD4 T-cell count was significantly associated with presence of HLA-A*24/*33, HLA-B*53, CCR5-CF2 and absence of HLA-A*01/*23 and CCR5-HHA. Lower 6-month CD4 T-cell count was associated with presence of HLA-A*24 and HLA-B*53, and absence of HLA-A*01 and HLA-B*07/*39. Moreover, lower 12-month CD4 T-cell count was significantly associated with presence of HLA-A*33, HLA-B*14, HLA-C*08, CCR5-CF2, and absence of HLA-B*07 and HLA-C*07.

conclusionSeveral host factors were significantly associated with disease progression in PHI subjects. Most results agree with previous studies performed in other groups. However, some genetic factor associations are being described for the first time, highlighting the importance of genetic studies at a local level.

Indexed as

ArgentinaBlotting, WesternCD4 Lymphocyte CountDisease ProgressionHaplotypesHIV SeropositivityHLA AntigensHost-Derived Cellular FactorsHumansPolymerase Chain ReactionPolymorphism, Restriction Fragment LengthReceptors, CCR5Viral LoadCCR5 protein, humanHLA AntigensHost-Derived Cellular FactorsReceptors, CCR5

Identifiers

PMID25406087
PMCPMC4236131
OpenAlexW2064489757

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.