Clonality of HIV-1– and HTLV-1–Infected Cells in Naturally Coinfected Individuals

  • Hiroo Katsuya
    Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan
  • Lucy B M Cook
    Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK
  • Aileen G Rowan
    Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK
  • Anat Melamed
    Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK
  • Jocelyn Turpin
    Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK
  • Jumpei Ito
    Division of Systems Virology, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo, Tokyo, Japan
  • Saiful Islam
    Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan
  • Paola Miyazato
    Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan
  • Benjy Jek Yang Tan
    Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan
  • Misaki Matsuo
    Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan
  • Toshikazu Miyakawa
    Department of Hematology, Rheumatology and Infectious Diseases, Kumamoto University of Medicine, Kumamoto, Japan
  • Hirotomo Nakata
    Department of Hematology, Rheumatology and Infectious Diseases, Kumamoto University of Medicine, Kumamoto, Japan
  • Shuzo Matsushita
    Clinical Retrovirology, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan
  • Graham P Taylor
    Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK
  • Charles R M Bangham
    Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK
  • Shinya Kimura
    Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan
  • Yorifumi Satou
    Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan

書誌事項

公開日
2021-04-12
資源種別
journal article
権利情報
  • https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model
DOI
  • 10.1093/infdis/jiab202
公開者
Oxford University Press (OUP)

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説明

<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p>Coinfection with human immunodeficiency virus type 1 (HIV-1) and human T-cell leukemia virus type 1 (HTLV-1) diminishes the value of the CD4+ T-cell count in diagnosing AIDS, and increases the rate of HTLV-1–associated myelopathy. It remains elusive how HIV-1/HTLV-1 coinfection is related to such characteristics. We investigated the mutual effect of HIV-1/HTLV-1 coinfection on their integration sites (ISs) and clonal expansion.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>We extracted DNA from longitudinal peripheral blood samples from 7 HIV-1/HTLV-1 coinfected, and 12 HIV-1 and 13 HTLV-1 monoinfected individuals. Proviral loads (PVL) were quantified using real-time polymerase chain reaction (PCR). Viral ISs and clonality were quantified by ligation-mediated PCR followed by high-throughput sequencing.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>PVL of both HIV-1 and HTLV-1 in coinfected individuals was significantly higher than that of the respective virus in monoinfected individuals. The degree of oligoclonality of both HIV-1– and HTLV-1–infected cells in coinfected individuals was also greater than in monoinfected subjects. ISs of HIV-1 in cases of coinfection were more frequently located in intergenic regions and transcriptionally silent regions, compared with HIV-1 monoinfected individuals.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>HIV-1/HTLV-1 coinfection makes an impact on the distribution of viral ISs and clonality of virus-infected cells and thus may alter the risks of both HTLV-1– and HIV-1–associated disease.</jats:p> </jats:sec>

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