ReviewFrontiers in immunology2017
Disarming Cellular Alarm Systems-Manipulation of Stress-Induced NKG2D Ligands by Human Herpesviruses.
Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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Who cites it
30 citing papers in PubMed.
- Reduced NK cell IFN-γ secretion and psychological stress are independently associated with herpes zoster.PloS one · 2018Trial
- Oral Innate Immunity and the Role of Oral Epithelial Cells.Advances in experimental medicine and biology · 2026Review
- The immunobiology of herpes simplex virus encephalitis and post-viral autoimmunity.Brain : a journal of neurology · 2024Review
- The HHV-6B U20 glycoprotein binds ULBP1, masking it from recognition by NKG2D and interfering with natural killer cell activation.Frontiers in immunology · 2024Article
- Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus.Current topics in microbiology and immunology · 2023Review
- Modulation of Apoptosis and Cell Death Pathways by Varicella-Zoster Virus.Current topics in microbiology and immunology · 2023Review
- Herpes simplex encephalitis following ChAdOx1 nCoV-19 vaccination: a case report and review of the literature.BMC infectious diseases · 2022Review
- Role of HLA-G in Viral Infections.Frontiers in immunology · 2022Review
- Article
- Review
- Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Herpes-like skin lesion after AstraZeneca vaccination for COVID-19: A case report.Clinical case reports · 2021Article
- NKG2D Natural Killer Cell Receptor-A Short Description and Potential Clinical Applications.Cells · 2021Review
- Review
- The HHV-6A Proteins U20 and U21 Target NKG2D Ligands to Escape Immune Recognition.Frontiers in immunology · 2021Article
- Genetic Variability of Human Cytomegalovirus Clinical Isolates Correlates With Altered Expression of Natural Killer Cell-Activating Ligands and IFN-γ.Frontiers in immunology · 2021Article
- COVID-19 and herpes zoster co-infection presenting with trigeminal neuropathy.European journal of neurology · 2020Article
- Human Metapneumovirus Escapes NK Cell Recognition through the Downregulation of Stress-Induced Ligands for NKG2D.Viruses · 2020Article
- Virus-Mediated Suppression of the Antigen Presentation Molecule MR1.Cell reports · 2020Article
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The coevolution of viruses and their hosts led to the repeated emergence of cellular alert signals and viral strategies to counteract them. The herpesvirus family of viruses displays the most sophisticated repertoire of immune escape mechanisms enabling infected cells to evade immune recognition and thereby maintain infection. The herpesvirus family consists of nine viruses that are capable of infecting humans: herpes simplex virus 1 and 2 (HSV-1, HSV-2), varicella zoster virus (VZV), Epstein-Barr virus (EBV), human cytomegalovirus (HCMV), roseoloviruses (HHV-6A, HHV-6B, and HHV-7), and Kaposi's-sarcoma-associated herpesvirus (KSHV). Most of these viruses are highly prevalent and infect a vast majority of the human population worldwide. Notably, research over the past 15 years has revealed that cellular ligands for the activating receptor natural-killer group 2, member D (NKG2D)-which is primarily expressed on natural killer (NK) cells-are common targets suppressed during viral infection, i.e., their surface expression is reduced in virtually all lytic herpesvirus infections by diverse mechanisms. Here, we review the viral mechanisms by which all herpesviruses known to date to downmodulate the expression of the NKG2D ligands. Also, in light of recent findings, we speculate about the importance of the emergence of eight different NKG2D ligands in humans and further allelic diversification during host and virus coevolution.
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