Murine Vβ3+ and Vβ7+ T Cell Subsets Are Specific Targets for the HERV-K18 Env Superantigen

Tai, Albert; Lin, Miao; Chang, Francesca; Chen, Gang; Hsiao, Francis C.; Sutkowski, Natalie; Huber, Brigitte

doi:10.4049/jimmunol.177.5.3178

Cited by 16 publications

(14 citation statements)

References 32 publications

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“…We further confirmed that HERV-K18 env is inducible in our double transgenic mice by anti-IgM treatment of the purified B cells (Fig. 2E) (26).…”

Section: Generation Of Hcd21/herv-k18 Double Transgenic Micesupporting

confidence: 68%

“…Thus, we produced double transgenic mice expressing hCD21 and HERV-K18 from bacteria artificial chromosomes (BACs). The HERV-K18 transgenic mice have been described elsewhere (26). To ensure that the hCD21 transgene is expressed from its native human regulatory elements and promoters, we selected a BAC, RP11-35C1, that contains hCD21 flanked by complement receptor 1 (CD35) and a hypothetical protein for injection into fertilized FVB eggs.…”

Section: Generation Of Hcd21/herv-k18 Double Transgenic Micementioning

confidence: 99%

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

Hsiao

Lin

Tai³

et al. 2006

The Journal of Immunology

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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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“…We further confirmed that HERV-K18 env is inducible in our double transgenic mice by anti-IgM treatment of the purified B cells (Fig. 2E) (26).…”

Section: Generation Of Hcd21/herv-k18 Double Transgenic Micesupporting

confidence: 68%

Section: Generation Of Hcd21/herv-k18 Double Transgenic Micementioning

confidence: 99%

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

Hsiao

Lin

Tai³

et al. 2006

The Journal of Immunology

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“…In addition, studies on the mechanism by which EBV stimulates HERV-K18 has implicated the EBV surface glycoprotein gp350 via signaling through CD21 (219) and the latent EBV proteins LMP-1 and LMP2A (471). HERV-K18 expression is also induced in B cells by immunoglobulin M cross-linking of CD40 on the cell surface (476). Therefore, current evidence now provides a more persuasive argument that the HERV-K18 SAg activity is genuine.…”

Section: Herv-k and Melanomamentioning

confidence: 93%

“…However, more recent work in mice transgenic for the HERV-K18 genomic locus has shown that murine V␤3 and V␤7 T-lymphocyte subsets are activated by HERV-K18 SAg in vivo (476). In addition, studies on the mechanism by which EBV stimulates HERV-K18 has implicated the EBV surface glycoprotein gp350 via signaling through CD21 (219) and the latent EBV proteins LMP-1 and LMP2A (471).…”

Section: Herv-k and Melanomamentioning

confidence: 99%

“…Indeed, an overtly pathogenic HERV would tend to be lost through negative selection (172). Nevertheless, this does not preclude the possibility that HERVs may comprise cofactors for disease in some circumstances, and recent work on specific proteins of HERV-K and HERV-W has provided new advances in this area (see below) (13,58,117,156,476).…”

Section: Hervs and Diseasementioning

confidence: 99%

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Human RNA “Rumor” Viruses: the Search for Novel Human Retroviruses in Chronic Disease

Voisset

Weiss

Griffiths

2008

Microbiol Mol Biol Rev

145

156

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SUMMARY Retroviruses are an important group of pathogens that cause a variety of diseases in humans and animals. Four human retroviruses are currently known, including human immunodeficiency virus type 1, which causes AIDS, and human T-lymphotropic virus type 1, which causes cancer and inflammatory disease. For many years, there have been sporadic reports of additional human retroviral infections, particularly in cancer and other chronic diseases. Unfortunately, many of these putative viruses remain unproven and controversial, and some retrovirologists have dismissed them as merely “human rumor viruses.” Work in this field was last reviewed in depth in 1984, and since then, the molecular techniques available for identifying and characterizing retroviruses have improved enormously in sensitivity. The advent of PCR in particular has dramatically enhanced our ability to detect novel viral sequences in human tissues. However, DNA amplification techniques have also increased the potential for false-positive detection due to contamination. In addition, the presence of many families of human endogenous retroviruses (HERVs) within our DNA can obstruct attempts to identify and validate novel human retroviruses. Here, we aim to bring together the data on “novel” retroviral infections in humans by critically examining the evidence for those putative viruses that have been linked with disease and the likelihood that they represent genuine human infections. We provide a background to the field and a discussion of potential confounding factors along with some technical guidelines. In addition, some of the difficulties associated with obtaining formal proof of causation for common or ubiquitous agents such as HERVs are discussed.

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Are human endogenous retroviruses pathogenic? An approach to testing the hypothesis

Young¹,

Stoye²,

Kassiotis³

2013

BioEssays

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A number of observations have led researchers to postulate that, despite being replication-defective, human endogenous retroviruses (HERVs) may have retained the potential to cause or contribute to disease. However, mechanisms of HERV pathogenicity might differ substantially from those of modern infectious retroviruses or of the infectious precursors of HERVs. Therefore, novel pathways of HERV involvement in disease pathogenesis should be investigated. Recent technological advances in sequencing and bioinformatics are making this task increasingly feasible. The accumulating knowledge of HERV biology may also facilitate the definition and general acceptance of criteria that establish HERV pathogenicity. Here, we explore possible mechanisms whereby HERVs may cause disease and examine the evidence that either has been or should be obtained in order to decisively address the pathogenic potential of HERVs.

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Murine Vβ3+ and Vβ7+ T Cell Subsets Are Specific Targets for the HERV-K18 Env Superantigen

Cited by 16 publications

References 32 publications

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

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

Human RNA “Rumor” Viruses: the Search for Novel Human Retroviruses in Chronic Disease

Are human endogenous retroviruses pathogenic? An approach to testing the hypothesis

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