Human endogenous retroviruses: transposable elements with potential?

Nelson, Paul N.; Hooley, Paul; Roden, Denise A.; Ejtehadi, Hora Davari; Rylance, Paul; Warren, Philip; Martin, Noreen; Murray, Paul G.

doi:10.1111/j.1365-2249.2004.02592.x

Cited by 79 publications

(78 citation statements)

References 76 publications

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“…HERVs possess two long-terminal repeats that flank a region containing group-specific Ag (gag), polymerase and other enzymes, and envelope (env) genes and no longer make virions due to inactivating mutations accumulated through evolution. HERVs are believed to have arisen from retroviruses that integrated into the genome of an ancestral germline (6). Located on the first chromosome HERV-K18 (1q23.1-q24) sits on the first intron of the cellular gene CD48 and has an opposite direction of transcription to that gene (7).…”

mentioning

confidence: 99%

“…HERV-K18 belongs to a class of retroelements, HERVs, that retain much of the genomic organization of modern day exogenous retroviruses such as HIV (6). HERVs possess two long-terminal repeats that flank a region containing group-specific Ag (gag), polymerase and other enzymes, and envelope (env) genes and no longer make virions due to inactivating mutations accumulated through evolution.…”

mentioning

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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confidence: 99%

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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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“…The etiology is unknown, although possible causes include viral triggers 1 . The latter may include human endogenous retroviral (HERV) families: HERV-K, HERV-L, ERV-9, and ERV-3 2,3 .…”

Section: To the Editormentioning

confidence: 99%

Endogenous Retrovirus Erv-3 Is Not Implicated in Rheumatoid Arthritis But May Provide a Biomarker for Osteoarthritis: Table 1

Nelson¹,

Davari-Ejtehadi²,

Nevill³

et al. 2010

J Rheumatol

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“…Increasing evidence shows links of HERVs with some human diseases, such as male infertility, schizophrenia, and cancer [6,[10][11]16]. Several studies reported expression of one or more HERVs in physiological or pathological conditions, in one or more body sites.…”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, similar to other animal species, the human genome contains remnants of many different kinds of retroviruses that are now endogenously transmitted and are hence called human endogenous retroviruses (HERVs) [4][5][6][7][8]. Apart from ~3% of coding sequences, for an estimate of 20,000-25,000 genes [9], the vast majority of DNA is composed of introns, pseudogenes, duplications, and by at least 50% repeat sequences (including genes that encode ribosomal components, minisatellite DNA, HERVs, and probably much more) [6,9,[10][11]. HERVs are grouped in 26-31 independently acquired families or lineages [12][13].…”

Section: Introductionmentioning

confidence: 99%

The aliens inside human DNA: HERV-W/MSRV/syncytin-1 endogenous retroviruses and neurodegeneration

Dolei

Uleri

Ibba

et al. 2015

J Infect Dev Ctries

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The human genome contains remnants of ancestral retroviruses now endogenously transmitted, called human endogenous retroviruses (HERVs). HERVs can be variably expressed, and both beneficial and detrimental effects have described. This review focuses on the MSRV and syncytin-1 HERV-W elements in relationship to neurodegeneration in view of their neuro-pathogenic and immune-pathogenic properties. Multiple sclerosis (MS) and a neurodegenerative disease (neuroAIDS) are reported in this review. In vivo studies in patients and controls for molecular epidemiology and follow-up studies are reviewed, along with in vitro cellular studies of the effects of treatments and of molecular mechanisms. HERV-W/MSRV has been repeatedly found in MS patients (in blood, spinal fluid, and brain samples), and MRSV presence/load strikingly parallels MS stages and active/remission phases, as well as therapy outcome. The DNA of MS patients has increased MSRVenv copies, while syncytin-1 copies are unchanged in controls. Presence of MSRV in the spinal fluid predicted the worst MS progression, ten years in advance. The Epstein-Barr virus (EBV) activates HERV-W/MSRV both in vitro and in vivo. With respect to neuroAIDS, the HIV transactivator of transcription (Tat) protein activates HERV-W/MSRV in monocytes/macrophages and astrocytes indirectly by interaction with TLR4 and induction of TNF. HERV-W/MSRV can be considered a biomarker for MS behavior and therapy outcome. Regarding MS pathogenesis, we postulate the possibility for EBV of an initial trigger of future MS, years later, and for MSRV of a direct role of effector of neuropathogenesis during MS. Additionally, HERV-W/MSR/syncytin-1 activation by HIV Tat could contribute to the HIV-related neurodegeneration.

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Human endogenous retroviruses: transposable elements with potential?

Cited by 79 publications

References 76 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

Endogenous Retrovirus Erv-3 Is Not Implicated in Rheumatoid Arthritis But May Provide a Biomarker for Osteoarthritis: Table 1

The aliens inside human DNA: HERV-W/MSRV/syncytin-1 endogenous retroviruses and neurodegeneration

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