Evidence map›Paper›PMID 38562862›Full record

ArticlebioRxiv : the preprint server for biology2024

Antigenic drift expands viral escape pathways from imprinted host humoral immunity.

Daniel P Maurer, Mya Vu, Aaron G Schmidt

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Mya Vu
Ragon Institute of MGH, MIT and Harvard · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An initial virus exposure can imprint antibodies such that future responses to antigenically drifted strains are dependent on the identity of the imprinting strain. Subsequent exposure to antigenically distinct strains followed by affinity maturation can guide immune responses toward generation of cross-reactive antibodies. How viruses evolve in turn to escape these imprinted broad antibody responses is unclear. Here, we used clonal antibody lineages from two human donors recognizing conserved influenza virus hemagglutinin (HA) epitopes to assess viral escape potential using deep mutational scanning. We show that even though antibody affinity maturation does restrict the number of potential escape routes in the imprinting strain through repositioning the antibody variable domains, escape is still readily observed in drifted strains and attributed to epistatic networks within HA. These data explain how influenza virus continues to evolve in the human population by escaping even broad antibody responses.

Identifiers

PMID38562862
PMCPMC10983950
OpenAlexW4393131099

What OpenQuestion holds

Textmetadata
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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.