ReviewBiochimica et biophysica acta2011
Human endogenous retroviruses and multiple sclerosis: innocent bystanders or disease determinants?
Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
71 citing papers in PubMed, 126 citations in OpenAlex.
- Review
- Asparaginase-like protein 1 and human endogenous retroviruses link immune and gene dysregulation in dementia.Frontiers in cellular and infection microbiology · 2026Article
- Immune System-Tumor Crosstalk Under Microgravity: Mechanistic Insights, Challenges, and Translational Perspectives.Cancers · 2025Review
- A unifying model for multiple sclerosis.Clinical and experimental medicine · 2025Review
- Unveiling the impact of simulated microgravity on HSV-1 infection, neuroinflammation, and endogenous retroviral activation in SH-SY5Y cells.Journal of neurovirology · 2025Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Transcriptional Upregulation of HERV-Viruses · 2025Article
- Activation of human endogenous retroviruses by Sox proteins induces cell apoptosis via the caspase-3 pathway.Frontiers in microbiology · 2025Article
- The potential protective role of carotenoids from saffron: A focus on endoplasmic reticulum stress-related organ damage.Food science & nutrition · 2024Review
- Species-Specific Transcription Factors Associated with Long Terminal Repeat Promoters of Endogenous Retroviruses: A Comprehensive Review.Biomolecules · 2024Review
- Immune response profiling of HERV-W envelope proteins in multiple sclerosis: potential biomarkers for disease progression.Frontiers in immunology · 2024Article
- ERVW-1 Activates ATF6-Mediated Unfolded Protein Response by Decreasing GANAB in Recent-Onset Schizophrenia.Viruses · 2023Article
- Association of Epstein-Barr Virus (EBV) and Human Endogenous Retroviruses (HERV) with Multiple Sclerosis in Northwest of Iran.International journal of inflammation · 2023Article
- Syncytin-1 nonfusogenic activities modulate inflammation and contribute to preeclampsia pathogenesis.Cellular and molecular life sciences : CMLS · 2022Review
- Differential expression of an endogenous retroviral element [HERV-K(HML-6)] is associated with reduced survival in glioblastoma patients.Scientific reports · 2022Article
- Epstein-Barr Virus Load Correlates with Multiple Sclerosis-Associated Retrovirus Envelope Expression.Biomedicines · 2022Article
- Transposable Elements in Pluripotent Stem Cells and Human Disease.Frontiers in genetics · 2022Review
- Human Endogenous Retroviruses as Gene Expression Regulators: Insights from Animal Models into Human Diseases.Molecules and cells · 2021Review
- Recombination Marks the Evolutionary Dynamics of a Recently Endogenized Retrovirus.Molecular biology and evolution · 2021Article
- HSV-1 and Endogenous Retroviruses as Risk Factors in Demyelination.International journal of molecular sciences · 2021Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human endogenous retroviruses (HERVs) constitute 5-8% of human genomic DNA and are replication incompetent despite expression of individual HERV genes from different chromosomal loci depending on the specific tissue. Several HERV genes have been detected as transcripts and proteins in the central nervous system, frequently in the context of neuroinflammation. The HERV-W family has received substantial attention in large part because of associations with diverse syndromes including multiple sclerosis (MS) and several psychiatric disorders. A HERV-W-related retroelement, multiple sclerosis retrovirus (MSRV), has been reported in MS patients to be both a biomarker as well as an effector of aberrant immune responses. HERV-H and HERV-K have also been implicated in MS and other neurological diseases but await delineation of their contributions to disease. The HERV-W envelope-encoded glycosylated protein, syncytin-1, is encoded by chromosome 7q21 and exhibits increased glial expression within MS lesions. Overexpression of syncytin-1 in glia induces endoplasmic reticulum stress leading to neuroinflammation and the induction of free radicals, which damage proximate cells. Syncytin-1's receptor, ASCT1 is a neutral amino acid transporter expressed on glia and is suppressed in white matter of MS patients. Of interest, antioxidants ameliorate syncytin-1's neuropathogenic effects raising the possibility of using these agents as therapeutics for neuroinflammatory diseases. Given the multiple insertion sites of HERV genes as complete and incomplete open reading frames, together with their differing capacity to be expressed and the complexities of individual HERVs as both disease markers and bioactive effectors, HERV biology is a compelling area for understanding neuropathogenic mechanisms and developing new therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.