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Tracking HIV-1 recombination to resolve its contribution to HIV-1 evolution in natural infection

Author

Listed:
  • Hongshuo Song

    (Duke University Medical Center
    Walter Reed Army Institute of Research)

  • Elena E. Giorgi

    (Los Alamos National Laboratory)

  • Vitaly V. Ganusov

    (University of Tennessee)

  • Fangping Cai

    (Duke University Medical Center)

  • Gayathri Athreya

    (University of Arizona)

  • Hyejin Yoon

    (Los Alamos National Laboratory)

  • Oana Carja

    (University of Pennsylvania)

  • Bhavna Hora

    (Duke University Medical Center)

  • Peter Hraber

    (Los Alamos National Laboratory)

  • Ethan Romero-Severson

    (Los Alamos National Laboratory)

  • Chunlai Jiang

    (Duke University Medical Center
    Jilin University)

  • Xiaojun Li

    (Duke University Medical Center)

  • Shuyi Wang

    (University of Pennsylvania)

  • Hui Li

    (University of Pennsylvania)

  • Jesus F. Salazar-Gonzalez

    (University of Alabama at Birmingham
    MRC/UVRI and LSHTM Uganda Research Unit)

  • Maria G. Salazar

    (University of Alabama at Birmingham)

  • Nilu Goonetilleke

    (University of North Carolina at Chapel Hill)

  • Brandon F. Keele

    (Frederick National Laboratory for Cancer Research)

  • David C. Montefiori

    (Duke University Medical Center)

  • Myron S. Cohen

    (University of North Carolina at Chapel Hill)

  • George M. Shaw

    (University of Pennsylvania
    University of Pennsylvania)

  • Beatrice H. Hahn

    (University of Pennsylvania
    University of Pennsylvania)

  • Andrew J. McMichael

    (University of Oxford)

  • Barton F. Haynes

    (Duke University Medical Center)

  • Bette Korber

    (Los Alamos National Laboratory)

  • Tanmoy Bhattacharya

    (Los Alamos National Laboratory
    Santa Fe Institute)

  • Feng Gao

    (Duke University Medical Center
    Jilin University)

Abstract

Recombination in HIV-1 is well documented, but its importance in the low-diversity setting of within-host diversification is less understood. Here we develop a novel computational tool (RAPR (Recombination Analysis PRogram)) to enable a detailed view of in vivo viral recombination during early infection, and we apply it to near-full-length HIV-1 genome sequences from longitudinal samples. Recombinant genomes rapidly replace transmitted/founder (T/F) lineages, with a median half-time of 27 days, increasing the genetic complexity of the viral population. We identify recombination hot and cold spots that differ from those observed in inter-subtype recombinants. Furthermore, RAPR analysis of longitudinal samples from an individual with well-characterized neutralizing antibody responses shows that recombination helps carry forward resistance-conferring mutations in the diversifying quasispecies. These findings provide insight into molecular mechanisms by which viral recombination contributes to HIV-1 persistence and immunopathogenesis and have implications for studies of HIV transmission and evolution in vivo.

Suggested Citation

  • Hongshuo Song & Elena E. Giorgi & Vitaly V. Ganusov & Fangping Cai & Gayathri Athreya & Hyejin Yoon & Oana Carja & Bhavna Hora & Peter Hraber & Ethan Romero-Severson & Chunlai Jiang & Xiaojun Li & Shu, 2018. "Tracking HIV-1 recombination to resolve its contribution to HIV-1 evolution in natural infection," Nature Communications, Nature, vol. 9(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04217-5
    DOI: 10.1038/s41467-018-04217-5
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