Evidence map›Paper›PMID 37325086›Full record

ArticleVirus evolution2023

Mutual information networks reveal evolutionary relationships within the influenza A virus polymerase.

Sarah Arcos, Alvin X Han, Aartjan J W Te Velthuis, Colin A Russell, Adam S Lauring

Open access · goldAbstract read
In one paragraph

Article in Virus evolution, 2023. 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
1.1field-weighted citation impact, top 22% 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. Article
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  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Sarah ArcosDepartment of Microbiology and Immunology, University of Michigan, 1150 West Medical Center Drive, 5641 Medical Science II, Ann Arbor, MI 48109, USA.ORCID https://orcid.org/0000-0002-3003-9040
Alvin X HanDepartment of Medical Microbiology and Infection Prevention, Amsterdam University Medical Center, Meibergdreef 9, Amsterdam 1105 AZ, The Netherlands.ORCID https://orcid.org/0000-0001-6281-8498
Aartjan J W Te VelthuisDepartment of Molecular Biology, Princeton University, 119 Lewis Thomas Laboratory, Washington Road, Princeton, NJ 08544, USA.ORCID https://orcid.org/0000-0002-5129-3953
Colin A RussellDepartment of Medical Microbiology and Infection Prevention, Amsterdam University Medical Center, Meibergdreef 9, Amsterdam 1105 AZ, The Netherlands.ORCID https://orcid.org/0000-0002-2113-162X
Adam S LauringDepartment of Microbiology and Immunology, University of Michigan, 1150 West Medical Center Drive, 5641 Medical Science II, Ann Arbor, MI 48109, USA.ORCID https://orcid.org/0000-0003-2906-8335
Amsterdam University Medical Centers · NLUniversity of Michigan · USPrinceton University · US

Funding

Molecular Mechanisms of Microbial Pathogenesis Training ProgramT32AI007528 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARRUTHERS, VERNON BRUCE · 1998 to 2024
$6.8M
Functional and genetic constraints on influenza virus replication and fidelityR01AI170520 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAURING, ADAM · 2022 to 2025
$2.4M
NIAID NIH HHS R01 AI170520NIAID NIH HHS T32 AI007528
6 · The paper itself

Abstract

The influenza A virus (IAV) RNA polymerase is an essential driver of IAV evolution. Mutations that the polymerase introduces into viral genome segments during replication are the ultimate source of genetic variation, including within the three subunits of the IAV polymerase (polymerase basic protein 2, polymerase basic protein 1, and polymerase acidic protein). Evolutionary analysis of the IAV polymerase is complicated, because changes in mutation rate, replication speed, and drug resistance involve epistatic interactions among its subunits. In order to study the evolution of the human seasonal H3N2 polymerase since the 1968 pandemic, we identified pairwise evolutionary relationships among ∼7000 H3N2 polymerase sequences using mutual information (MI), which measures the information gained about the identity of one residue when a second residue is known. To account for uneven sampling of viral sequences over time, we developed a weighted MI (wMI) metric and demonstrate that wMI outperforms raw MI through simulations using a well-sampled severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) dataset. We then constructed wMI networks of the H3N2 polymerase to extend the inherently pairwise wMI statistic to encompass relationships among larger groups of residues. We included hemagglutinin (HA) in the wMI network to distinguish between functional wMI relationships within the polymerase and those potentially due to hitch-hiking on antigenic changes in HA. The wMI networks reveal coevolutionary relationships among residues with roles in replication and encapsidation. Inclusion of HA highlighted polymerase-only subgraphs containing residues with roles in the enzymatic functions of the polymerase and host adaptability. This work provides insight into the factors that drive and constrain the rapid evolution of influenza viruses.

Indexed as

Influenza Avirusinformation theoryRNA-dependent RNA polymerasevirus evolution

Identifiers

PMID37325086
PMCPMC10263469
OpenAlexW4378710418

What OpenQuestion holds

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LicenceCC BY-NC
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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.