Evidence map›Paper›PMID 35145025›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Evolution during primary HIV infection does not require adaptive immune selection.

David A Swan, Morgane Rolland, Joshua T Herbeck, Joshua T Schiffer, Daniel B Reeves

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. 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

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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Recurrent mutations drive rapid HIV escape from two broadly neutralizing antibodies in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Modelling HIV-1 control and remission.NPJ systems biology and applications · 2024
    Review
  11. Article
  12. Review
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

5 authors.

David A SwanVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.ORCID 0000-0002-3295-0372
Morgane RollandUS Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, MD 20910.ORCID 0000-0003-3650-8490
Joshua T HerbeckInternational Clinical Research Center, Department of Global Health, University of Washington, Seattle, WA 98195.
Joshua T SchifferVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.ORCID 0000-0002-2598-1621
Daniel B ReevesVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109; dreeves@fredhutch.org.ORCID 0000-0001-5684-9538

Funding

SDMC: HIV Vaccine Trials NetworkUM1AI068635 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Peter B. Gilbert, Yunda Huang · 2011 to 2026
$385.9M
Simulating persistence and elimination of the HIV reservoirK25AI155224 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI REEVES, DANIEL · 2020 to 2024
$581k
NIAID NIH HHS K25 AI155224NIAID NIH HHS UM1 AI068635
6 · The paper itself

Abstract

Modern HIV research depends crucially on both viral sequencing and population measurements. To directly link mechanistic biological processes and evolutionary dynamics during HIV infection, we developed multiple within-host phylodynamic models of HIV primary infection for comparative validation against viral load and evolutionary dynamics data. The optimal model of primary infection required no positive selection, suggesting that the host adaptive immune system reduces viral load but surprisingly does not drive observed viral evolution. Rather, the fitness (infectivity) of mutant variants is drawn from an exponential distribution in which most variants are slightly less infectious than their parents (nearly neutral evolution). This distribution was not largely different from either in vivo fitness distributions recorded beyond primary infection or in vitro distributions that are observed without adaptive immunity, suggesting the intrinsic viral fitness distribution may drive evolution. Simulated phylogenetic trees also agree with independent data and illuminate how phylogenetic inference must consider viral and immune-cell population dynamics to gain accurate mechanistic insights.

Indexed as

PhylogenyViral LoadAdaptation, PhysiologicalGenetic FitnessHIV-1HIV InfectionsHumansModels, GeneticMutationReproducibility of ResultsHIV primary infectionphylodynamicsphylogeneticsviral dynamics modelingviral evolution

Identifiers

PMID35145025
PMCPMC8851487

What OpenQuestion holds

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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.