ArticlePloS one2013
Human herpesvirus 6A partially suppresses functional properties of DC without viral replication.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Studying the Interactions of U24 from HHV-6 in Order to Further Elucidate Its Potential Role in MS.Viruses · 2022Article
- Human Herpesvirus 6A Is a Risk Factor for Multiple Sclerosis.Frontiers in immunology · 2022Review
- HLA Class I Upregulation and Antiviral Immune Responses in Graves Disease.The Journal of clinical endocrinology and metabolism · 2021Article
- Epstein-Barr virus infection after adolescence and human herpesvirus 6A as risk factors for multiple sclerosis.European journal of neurology · 2021Article
- Human Herpesvirus 6A Induces Dendritic Cell Death and HMGB1 Release without Virus Replication.Pathogens (Basel, Switzerland) · 2021Article
- Phenotypic and Functional Differences between Human Herpesvirus 6- and Human Cytomegalovirus-Specific T Cells.Journal of virology · 2019Article
- Modulatory effects on dendritic cells by human herpesvirus 6.Frontiers in microbiology · 2015Review
- Human herpesviruses-encoded dUTPases: a family of proteins that modulate dendritic cell function and innate immunity.Frontiers in microbiology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human herpesvirus 6A (HHV-6A) is a common virus with a worldwide distribution that has been associated with multiple sclerosis. Whether HHV-6A can replicate in dendritic cells (DC) and how the infection might modulate the functional properties of the cell are currently not well known and need further investigations. Here, we show that a non-productive infection of HHV-6A in DC leads to the up-regulation of HLA-ABC, via autocrine IFN-α signaling, as well as the up-regulation of HLA-DR and CD86. However, HHV-6A exposure reduces IL-8 secretion by DC and their capacity to stimulate allogenic T cell proliferation. The ability to suppress DC functions important for activation of innate and adaptive immune responses might be one successful strategy by which HHV-6A avoids the induction of appropriate host defense mechanisms, and thus facilitating persistent infection.
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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.