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


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
18 01 2022
Historique:
received: 22 12 2020
accepted: 11 04 2021
pubmed: 13 4 2021
medline: 16 2 2022
entrez: 12 4 2021
Statut: ppublish

Résumé

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. 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. 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. 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.

Sections du résumé

BACKGROUND
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.
METHODS
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.
RESULTS
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.
CONCLUSIONS
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.

Identifiants

pubmed: 33844021
pii: 6222242
doi: 10.1093/infdis/jiab202
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

317-326

Subventions

Organisme : Medical Research Council
ID : MR/K019090/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/T029005/1
Pays : United Kingdom

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

Auteurs

Hiroo Katsuya (H)

Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.
Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.

Lucy B M Cook (LBM)

Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK.

Aileen G Rowan (AG)

Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK.

Anat Melamed (A)

Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK.

Jocelyn Turpin (J)

Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK.

Jumpei Ito (J)

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 (S)

Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.

Paola Miyazato (P)

Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.

Benjy Jek Yang Tan (B)

Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.

Misaki Matsuo (M)

Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.

Toshikazu Miyakawa (T)

Department of Hematology, Rheumatology and Infectious Diseases, Kumamoto University of Medicine, Kumamoto, Japan.

Hirotomo Nakata (H)

Department of Hematology, Rheumatology and Infectious Diseases, Kumamoto University of Medicine, Kumamoto, Japan.

Shuzo Matsushita (S)

Clinical Retrovirology, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.

Graham P Taylor (GP)

Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK.

Charles R M Bangham (CRM)

Department of Infectious Diseases, Faculty of Medicine, Imperial College London, London, UK.

Shinya Kimura (S)

Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.

Yorifumi Satou (Y)

Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.

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Classifications MeSH