Evidence map›Paper›PMID 41561446›Full record

ArticleVirus evolution2026

Single genome amplification and molecular cloning of HIV-1 populations in acute HIV-1 infection: implications for studies on HIV-1 diversity and evolutionary rate.

Anthony Y Y Hsieh, Amin S Hassan, Jamirah Nazziwa, Lovisa Lindquist, Sara Karlson, Jonathan Hare, Anatoli Kamali, Etienne Karita, William Kilembe, Matt A Price and 8 more

Abstract read
In one paragraph

Article in Virus evolution, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

18 authors.

Anthony Y Y HsiehCentre for Immuno-Oncology, University of Oxford, Nuffield Department of Medicine, Old Road Campus Research Building, Roosevelt Drive, Oxford, OX3 7DQ, United Kingdom.
Amin S HassanKEMRI/Wellcome Trust Research Programme, Kilifi, Kenya.
Jamirah NazziwaDepartment of Translational Medicine, Wallenberg Lab, plan 6, Inga Marie Nilssons gata 53, Lund University, 214 28 Malmö, Sweden.
Lovisa LindquistDepartment of Translational Medicine, Wallenberg Lab, plan 6, Inga Marie Nilssons gata 53, Lund University, 214 28 Malmö, Sweden.
Sara KarlsonDepartment of Translational Medicine, Wallenberg Lab, plan 6, Inga Marie Nilssons gata 53, Lund University, 214 28 Malmö, Sweden.
Jonathan HareIAVI  New York, 125 Broad Street, 9th Floor, New York, NY 10004, United States.
Anatoli KamaliIAVI  New York, 125 Broad Street, 9th Floor, New York, NY 10004, United States.
Etienne KaritaCenter for Family Health Research, 57 KK 19 Avenue, Building 2, Kigali, Rwanda.
William KilembeCenter for Family Health Research, B22/F737 Mwembelelo Road, Emmasdale, Lusaka, Zambia.ORCID https://orcid.org/0000-0002-9012-7325
Matt A PriceIAVI  New York, 125 Broad Street, 9th Floor, New York, NY 10004, United States.
Per BjörkmanDepartment of Translational Medicine, Wallenberg Lab, plan 6, Inga Marie Nilssons gata 53, Lund University, 214 28 Malmö, Sweden.
Pontiano KaleebuUganda Research Unit, Medical Research Council/Uganda Virus Research Institute and London School of Hygiene and Tropical Medicine, Plot 51-59 Nakiwogo Road, PO Box 49, Entebbe, Uganda.
Susan AllenCenter for Family Health Research, B22/F737 Mwembelelo Road, Emmasdale, Lusaka, Zambia.
Eric HunterCenter for Family Health Research, B22/F737 Mwembelelo Road, Emmasdale, Lusaka, Zambia.
Jill GilmourDepartment of Infectious Diseases, Infection and Immunity, Faculty of Medicine, Imperial College, Exhibition Road, South Kensington, London, SW7 2AZ, United Kingdom.
Sarah L Rowland-JonesCentre for Immuno-Oncology, University of Oxford, Nuffield Department of Medicine, Old Road Campus Research Building, Roosevelt Drive, Oxford, OX3 7DQ, United Kingdom.
Eduard J SandersKEMRI/Wellcome Trust Research Programme, Kilifi, Kenya.
Joakim EsbjörnssonCentre for Immuno-Oncology, University of Oxford, Nuffield Department of Medicine, Old Road Campus Research Building, Roosevelt Drive, Oxford, OX3 7DQ, United Kingdom.ORCID https://orcid.org/0000-0002-6088-7796

Funding

Deciphering the impact of sex in early subtype C HIV infection and during HARTR01AI172740 · NIAID · EMORY UNIVERSITY · PI Eric Hunter · 2022 to 2026
$4.3M
NIAID NIH HHS R01 AI172740
6 · The paper itself

Abstract

Background: Human immunodeficiency virus type 1 (HIV-1) is one of the fastest-evolving human pathogens. Understanding HIV-1 transmission, within-host adaptation, and evolutionary dynamics is pivotal for development of interventions and vaccines. HIV-1 infection is generally caused by a single transmitted founder virus (TFV), and TFV sequences are typically obtained using single genome amplification (SGA). However, suboptimal sample quality can cause sequencing failures, representing considerable losses considering the scarcity of acute HIV-1 infection (AHI) samples. Sequencing failures may be mitigated by molecular cloning (MC), which can be less vulnerable to sample quality but more susceptible to polymerase chain reaction (PCR) errors. Here, we explore the feasibility of supplementing SGA with MC data using samples from clinical and research cohorts to determine whether sequence diversity and evolutionary rate estimates are comparable between the techniques. Methods: Plasma samples were selected from participants with documented AHI from an East African research cohort (the International AIDS Vaccine Initiative, 2006-2011) and a clinical cohort from Sweden (1983-2011). SGA and MC sequencing were done on the HIV-1 Results: One hundred participants (median age 30.3 years, 15% female), contributing 350 samples from four longitudinal time points, 10-540 days post-infection, met the inclusion criteria. SGA succeeded on 90% of research cohort and 48% of clinical cohort samples. Comparative analysis of linked SGA and MC data from 10 samples indicated that approximately eight sequences were necessary for diversity estimates. Consistently higher sequence diversity was observed among MC relative to SGA sequences (median [IQR]: 0.009 [0.003, 0.015] and 0.004 [0.001, 0.012] substitutions/site, Conclusion: MC data is a suitable supplement for SGA-based HIV-1 studies to preserve the value of precious samples for analysis of evolutionary rate, but not for sequence diversity.

Indexed as

acute HIV-1 infectionHIV-1HIV-1 diversityHIV-1 evolutionmolecular cloningphylogeneticssingle genome amplificationtransmitted founder virus

Identifiers

PMID41561446
PMCPMC12815262

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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.