Evidence map›Paper›PMID 37214809›Full record

ArticlebioRxiv : the preprint server for biology2023

Within-host rhinovirus evolution in upper and lower respiratory tract highlights capsid variability and mutation-independent compartmentalization.

Negar Makhsous, Stephanie Goya, Carlos Avendaño, Jason Rupp, Jane Kuypers, Keith R Jerome, Michael Boeckh, Alpana Waghmare, Alexander L Greninger

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Negar MakhsousDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
Stephanie GoyaDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
Carlos AvendañoDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
Jason RuppDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
Jane KuypersDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
Keith R JeromeDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
Michael BoeckhVaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, 98109, USA.
Alpana WaghmareVaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, 98109, USA.
Alexander L GreningerDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, 98102, USA.
University of Washington · US

Funding

Viral and Host Biomarkers of Human Rhinovirus Disease Severity in TransplantationK23AI114844 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI WAGHMARE, ALPANA AMALKANT · 2015 to 2019
$897k
NIAID NIH HHS K23 AI114844
6 · The paper itself

Abstract

Background: Human rhinovirus (HRV) infections can progress from the upper (URT) to lower (LRT) respiratory tract in immunocompromised individuals, causing high rates of fatal pneumonia. Little is known about how HRV evolves within hosts during infection. Methods: We sequenced HRV complete genomes from 12 hematopoietic cell transplant patients with prolonged infection for up to 190 days from both URT (nasal wash, NW) and LRT (bronchoalveolar lavage, BAL) specimens. Metagenomic (mNGS) and amplicon-based NGS were used to study the emergence and evolution of intra-host single nucleotide variants (iSNVs). Results: Identical HRV intra-host populations in matched NW and BAL specimens indicated no genetic adaptation is required for HRV to progress from URT to LRT. Microbial composition between matched NW and BAL confirmed no cross-contamination during sampling procedure. Coding iSNVs were 2.3-fold more prevalent in capsid over non-structural genes, adjusted for length. iSNVs modeled onto HRV capsid structures were significantly more likely to be found in surface residues, but were not preferentially located in known HRV neutralizing antibody epitopes. Newly emergent, serotype-matched iSNV haplotypes from immunocompromised individuals from 2008-2010 could be detected in Seattle-area community HRV sequences from 2020-2021. Conclusion: HRV infections in immunocompromised hosts can progress from URT to LRT with no specific evolutionary requirement. Capsid proteins carry the highest variability and emergent mutations can be detected in other, including future, HRV sequences.

Identifiers

PMID37214809
PMCPMC10197658
OpenAlexW4376286348

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.