Endogenization and excision of human herpesvirus 6 in human genomes.


Journal

PLoS genetics
ISSN: 1553-7404
Titre abrégé: PLoS Genet
Pays: United States
ID NLM: 101239074

Informations de publication

Date de publication:
08 2020
Historique:
received: 13 04 2020
accepted: 07 06 2020
revised: 20 08 2020
pubmed: 11 8 2020
medline: 24 9 2020
entrez: 11 8 2020
Statut: epublish

Résumé

Sequences homologous to human herpesvirus 6 (HHV-6) are integrated within the nuclear genome of about 1% of humans, but it is not clear how this came about. It is also uncertain whether integrated HHV-6 can reactivate into an infectious virus. HHV-6 integrates into telomeres, and this has recently been associated with polymorphisms affecting MOV10L1. MOV10L1 is located on the subtelomere of chromosome 22q (chr22q) and is required to make PIWI-interacting RNAs (piRNAs). As piRNAs block germline integration of transposons, piRNA-mediated repression of HHV-6 integration has been proposed to explain this association. In vitro, recombination of the HHV-6 genome along its terminal direct repeats (DRs) leads to excision from the telomere and viral reactivation, but the expected "solo-DR scar" has not been described in vivo. Here we screened for integrated HHV-6 in 7,485 Japanese subjects using whole-genome sequencing (WGS). Integrated HHV-6 was associated with polymorphisms on chr22q. However, in contrast to prior work, we find that the reported MOV10L1 polymorphism is physically linked to an ancient endogenous HHV-6A variant integrated into the telomere of chr22q in East Asians. Unexpectedly, an HHV-6B variant has also endogenized in chr22q; two endogenous HHV-6 variants at this locus thus account for 72% of all integrated HHV-6 in Japan. We also report human genomes carrying only one portion of the HHV-6B genome, a solo-DR, supporting in vivo excision and possible viral reactivation. Together these results explain the recently-reported association between integrated HHV-6 and MOV10L1/piRNAs, suggest potential exaptation of HHV-6 in its coevolution with human chr22q, and clarify the evolution and risk of reactivation of the only intact (non-retro)viral genome known to be present in human germlines.

Identifiants

pubmed: 32776928
doi: 10.1371/journal.pgen.1008915
pii: PGENETICS-D-20-00558
pmc: PMC7444522
doi:

Substances chimiques

RNA, Small Interfering 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1008915

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Xiaoxi Liu (X)

Genome Immunobiology RIKEN Hakubi Research Team, RIKEN Cluster for Pioneering Research and RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Shunichi Kosugi (S)

Laboratory for Statistical and Translational Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Rie Koide (R)

Genome Immunobiology RIKEN Hakubi Research Team, RIKEN Cluster for Pioneering Research and RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Yoshiki Kawamura (Y)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.

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.

Hiroki Miura (H)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.

Nana Matoba (N)

Laboratory for Statistical and Translational Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Motomichi Matsuzaki (M)

Statistical Genetics Team, RIKEN Center for Advanced Intelligence Project, Tokyo, Japan.

Masashi Fujita (M)

Laboratory for Cancer Genomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Anselmo Jiro Kamada (AJ)

Genome Immunobiology RIKEN Hakubi Research Team, RIKEN Cluster for Pioneering Research and RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Hidewaki Nakagawa (H)

Laboratory for Cancer Genomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Gen Tamiya (G)

Statistical Genetics Team, RIKEN Center for Advanced Intelligence Project, Tokyo, Japan.

Koichi Matsuda (K)

Laboratory of Molecular Medicine, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Laboratory for Clinical Genome Sequencing, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.

Yoshinori Murakami (Y)

Division of Molecular Pathology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Michiaki Kubo (M)

RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Amr Aswad (A)

Institut für Virologie, Freie Universität Berlin, Berlin, Germany.

Kei Sato (K)

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.

Yukihide Momozawa (Y)

Laboratory for Genotyping Development, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Jun Ohashi (J)

Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.

Chikashi Terao (C)

Laboratory for Statistical and Translational Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Tetsushi Yoshikawa (T)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.

Nicholas F Parrish (NF)

Genome Immunobiology RIKEN Hakubi Research Team, RIKEN Cluster for Pioneering Research and RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Yoichiro Kamatani (Y)

Laboratory for Statistical and Translational Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Laboratory of Complex Trait Genomics, Graduate School of Frontier Sciences, The University of Tokyo, Japan.

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