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Cited by 98Viral-associated cancers and disordersCytomegalovirus and herpesvirus researchHerpesvirus Infections and Treatments

The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.

Cutting Edge: Epstein-Barr Virus Transactivates the HERV-K18 Superantigen by Docking to the Human Complement Receptor 2 (CD21) on Primary B Cells

Hsiao, Francis C, Lin, Miao, Tai, Albert, Chen, Gang, Huber, Brigitte T·2006·The Journal of Immunology
DOI 10.4049/jimmunol.177.4.2056
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Abstract

EBV, a ubiquitous human herpesvirus, is the causative agent of infectious mononucleosis and is associated with many carcinomas. We have previously shown that the EBV latent genes LMP-1 and LMP-2A (for latent membrane proteins 1 and 2A), transactivate a human endogenous retrovirus (HERV), HERV-K18, in infected B lymphocytes. The envelope (Env) protein of HERV-K18 encodes a superantigen that strongly stimulates a large number of T cells. In this study we report that HERV-K18 env is transactivated even earlier in the infection process, before the establishment of latency; namely, we found that EBV, through its interaction with its cellular receptor CD21, induces the HERV-K18 env gene in resting B lymphocytes. This transactivation is direct and immediate, as up-regulation of transcripts can be detected within 30 min after EBV exposure. Thus, EBV binding to human CD21 on resting B cells triggers the expression of an endogenous superantigen. The biological significance of this superantigen expression for the EBV life cycle is discussed.

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Crossref · 10.4049/jimmunol.177.4.2056

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29 of 29 references verified0 citation errors · 0 not checkable

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  • Transcription of a copy of HERV-K18 can be induced by several stimuli that activate B cells, including EBV infection.

    “Owing to integration into the first intron of the CD48 gene, encoding a lymphocyte-expressed member of the CD2 subfamily of immunoglobulin-like receptors, transcription of a copy of HERV-K18 can be induced by several stimuli that activate B cells, including EBV infection 47,48.”

    From Are human endogenous retroviruses pathogenic? An approach to testing the hypothesis (2013) · cites this paper as [47]

Citations

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Metadata

Authors
Hsiao, F. C., Lin, M., Tai, A., Chen, G., & Huber, B. T.
Affiliations
Tufts University (US)
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2006-08
Volume
177
Issue
4
Pages
2056-2060
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.177.4.2056
OpenAlex
W2125969570
Cited by
93
References
29
Citations by year
2026: 2 · 2025: 2 · 2024: 8 · 2023: 3 · 2022: 5 · 2021: 8 · 2020: 3 · 2019: 2 · 2018: 6 · 2016: 3 · 2015: 3 · 2014: 7 · 2013: 8 · 2012: 4
FWCI
3.30
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Allergy and Infectious Diseases (R01 AI14910, R01AI014910)
  • National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK-34928, P30DK034928)
Topics
  • Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
  • Health Sciences › Medicine › Epidemiology › Cytomegalovirus and herpesvirus research
  • Health Sciences › Medicine › Infectious Diseases › Herpesvirus Infections and Treatments
Keywords
Epstein-Barr virus, superantigens, CD21, CR2, endogenous retroviruses, B cells, viral transactivation, viral envelope proteins, latent membrane protein 1, LMP2A, T cell activation
MeSH terms
Animals, Cells, Cultured, Herpesvirus 4, Human, Humans, Membrane Proteins, Mice, Transgenic, Palatine Tonsil, Virus Activation, Transcriptional Activation, B-Lymphocyte Subsets, Receptors, Complement 3d, Superantigens, Mice

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