CD134 is a cellular receptor specific for human herpesvirus-6B entry

Human herpesvirus-6B (HHV-6B) is a T lymphotropic β-herpesvirus that is clearly distinct from human herpesvirus-6A (HHV-6A) according to molecular biological features. The International Committee on Taxonomy of Viruses recently classified HHV-6B as a separate species. The primary HHV-6B infection ca...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2013-05, Vol.110 (22), p.9096-9099
Main Authors: Tang, Huamin, Serada, Satoshi, Kawabata, Akiko, Ota, Megumi, Hayashi, Emi, Naka, Tetsuji, Yamanishi, Koichi, Mori, Yasuko
Format: Article
Language:English
Subjects:
Antibodies
Biological Sciences
Cell lines
Cellular receptors
Flow Cytometry
Gene expression
Glycoproteins
HEK293 Cells
Herpes viruses
Herpesviridae
Herpesvirus 6, Human - metabolism
Herpesvirus 6, Human - physiology
Human herpesvirus 6
Humans
Infections
Pathogenesis
Plasmids
Plasmids - genetics
Receptors
Receptors, OX40 - metabolism
T cell receptors
T lymphocytes
T-Lymphocytes - metabolism
T-Lymphocytes - virology
Viral Fusion Proteins - metabolism
Virus Internalization
Viruses
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Summary:Human herpesvirus-6B (HHV-6B) is a T lymphotropic β-herpesvirus that is clearly distinct from human herpesvirus-6A (HHV-6A) according to molecular biological features. The International Committee on Taxonomy of Viruses recently classified HHV-6B as a separate species. The primary HHV-6B infection causes exanthem subitum and is sometimes associated with severe encephalopathy. More than 90% of the general population is infected with HHV-6B during childhood, and the virus remains throughout life as a latent infection. HHV-6B reactivation causes encephalitis in immunosuppressed patients. The cellular receptor for HHV-6A entry was identified as human CD46, but the receptor for HHV-6B has not been clear. Here we found that CD134, a member of the TNF receptor superfamily, functions as a specific entry receptor for HHV-6B. A T-cell line that is normally nonpermissive for HHV-6B infection became highly susceptible to infection when CD134 was overexpressed. CD134 was down-regulated in HHV-6B–infected T cells. Soluble CD134 interacted with the HHV-6B glycoprotein complex that serves as a viral ligand for cellular receptor, which inhibited HHV-6B but not HHV-6A infection in target cells. The identification of CD134 as an HHV-6B specific entry receptor provides important insight into understanding HHV-6B entry and its pathogenesis.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1305187110