Evidence map›Paper›PMID 28535768›Full record

ArticleRetrovirology2017

Parent-offspring regression to estimate the heritability of an HIV-1 trait in a realistic setup.

Nadine Bachmann, Teja Turk, Claus Kadelka, Alex Marzel, Mohaned Shilaih, Jürg Böni, Vincent Aubert, Thomas Klimkait, Gabriel E Leventhal, Huldrych F Günthard and 2 more

Abstract read
In one paragraph

Article in Retrovirology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

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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

12 citing papers in PubMed.

  1. Article
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  9. International journal of environmental research and public health · 2019
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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

12 authors.

Nadine BachmannDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland. nadine.bachmann2@usz.ch.ORCID 0000-0002-7303-9542
Teja TurkDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland.
Claus KadelkaDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland.
Alex MarzelDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland.
Mohaned ShilaihDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland.
Jürg BöniInstitute of Medical Virology, University of Zurich, Zurich, Switzerland.
Vincent AubertDivisions of Immunology and Allergy, University Hospital Lausanne, Lausanne, Switzerland.
Thomas KlimkaitMolecular Virology, Department Biomedicine - Petersplatz, University of Basel, Basel, Switzerland.
Gabriel E LeventhalDepartment of Environmental Systems Science, ETH Zurich, Zurich, Switzerland.
Huldrych F GünthardDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland.
Roger KouyosDepartment of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland. roger.kouyos@usz.ch.
Swiss HIV Cohort Study

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParent-offspring (PO) regression is a central tool to determine the heritability of phenotypic traits; i.e., the relative extent to which those traits are controlled by genetic factors. The applicability of PO regression to viral traits is unclear because the direction of viral transmission-who is the donor (parent) and who is the recipient (offspring)-is typically unknown and viral phylogenies are sparsely sampled.

methodsWe assessed the applicability of PO regression in a realistic setting using Ornstein-Uhlenbeck simulated data on phylogenies built from 11,442 Swiss HIV Cohort Study (SHCS) partial pol sequences and set-point viral load (SPVL) data from 3293 patients.

resultsWe found that the misidentification of donor and recipient plays a minor role in estimating heritability and showed that sparse sampling does not influence the mean heritability estimated by PO regression. A mixed-effect model approach yielded the same heritability as PO regression but could be extended to clusters of size greater than 2 and allowed for the correction of confounding effects. Finally, we used both methods to estimate SPVL heritability in the SHCS. We employed a wide range of transmission pair criteria to measure heritability and found a strong dependence of the heritability estimates to these criteria. For the most conservative genetic distance criteria, for which heritability estimates are conceptually expected to be closest to true heritability, we found estimates ranging from 32 to 46% across different bootstrap criteria. For less conservative distance criteria, we found estimates ranging down to 8%. All estimates did not change substantially after adjusting for host-demographic factors in the mixed-effect model (±2%).

conclusionsFor conservative transmission pair criteria, both PO regression and mixed-effect models are flexible and robust tools to estimate the contribution of viral genetic effects to viral traits under real-world settings. Overall, we find a strong effect of viral genetics on SPVL that is not confounded by host demographics.

Indexed as

Viral LoadCohort StudiesComputer SimulationFemaleGenes, polGenotypeHIV-1HIV InfectionsHumansMalePhenotypePhylogenyRegression AnalysisHeritabilityHIV-1Mixed-effect modelOrnstein–Uhlenbeck processParent-offspring regressionSet-point viral load

Identifiers

PMID28535768
PMCPMC5442860

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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.