An Animal Model That Mimics Human Herpesvirus 6B Pathogenesis.


Journal

Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724

Informations de publication

Date de publication:
28 02 2020
Historique:
received: 29 10 2019
accepted: 12 12 2019
pubmed: 20 12 2019
medline: 4 9 2020
entrez: 20 12 2019
Statut: epublish

Résumé

Human herpesvirus 6B (HHV-6B), a T-lymphotropic virus, infects almost exclusively humans. An animal model of HHV-6B has not been available. Here, we report the first animal model to mimic HHV-6B pathogenesis; the model is based on humanized mice in which human immune cells were engrafted and maintained. For HHV-6B replication, adequate human T-cell activation (which becomes susceptible to HHV-6B) is necessary in this murine model. Here, we found that an additional transfer of human mononuclear cells to humanized mice resulted in an explosive proliferation of human activated T cells, which could be representative of graft-versus-host disease (GVHD) because the primary transfer of human cells was not sufficient to increase the number and ratio of human T cells. Mice infected with HHV-6B became weak and/or died approximately 7 to 14 days later. Quantitative PCR analysis revealed that the spleen and lungs were the major sites of HHV-6B replication in this model, and this was corroborated by the detection of viral proteins in these organs. Histological analysis also revealed the presence of megakaryocytes, indicating HHV-6B infection. Multiplex analysis of cytokines/chemokines in sera from the infected mice showed secretions of human cytokines/chemokines as reported for both

Identifiants

pubmed: 31852793
pii: JVI.01851-19
doi: 10.1128/JVI.01851-19
pmc: PMC7158738
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2020 American Society for Microbiology.

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Auteurs

Bochao Wang (B)

Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.

Yasuyuki Saito (Y)

Division of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.

Mitsuhiro Nishimura (M)

Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.

Zhenxiao Ren (Z)

Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.

Lidya Handayani Tjan (LH)

Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.

Alaa Refaat (A)

Division of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.

Rie Iida-Norita (R)

Division of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.

Ryuko Tsukamoto (R)

Department of Diagnostic Pathology, Kobe University Hospital, Kobe, Japan.

Masato Komatsu (M)

Department of Diagnostic Pathology, Kobe University Hospital, Kobe, Japan.

Tomoo Itoh (T)

Department of Diagnostic Pathology, Kobe University Hospital, Kobe, Japan.

Takashi Matozaki (T)

Division of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan.

Yasuko Mori (Y)

Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan ymori@med.kobe-u.ac.jp.

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